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Question 1: Define Shortened dental arch and mention 3 cases where the concept doesn’t
apply?

Shortened dental arch is defined by Käyser, A. F (1981) as:

A dentition where most posterior teeth are missing. This condition is frequently seen as molars
are often lost by caries and periodontal diseases.

Classified into 6 classes, according to the degree and the symmetry of the shortened condition:
Class I, Normal 11-12(Occlusal units =pairs of occluding posterior teeth, 1 molar = 2premolars)
Class Il, Asymmetric: (a) 6-8 OU (b) 4-5 OU
Class III, Symmetric: (a) 7-8 OU (b) 3-4 OU
Class IV is the extremely shortened group 0-2 OU

Results: Subjects started complaining about their masticatory function when the number of OU was
less than 4 in symmetrically SDA and less than 6 in asymmetrically SDA.

Kayser concluded from his study of 90 subjects with SDA for more than 2 years that there is
sufficient adaptive capacity in SDA when at least 4 occlusal units are left, preferably in a
symmetrical position. (premolar dentition).

Witter et al (1999), in a 6- year follow-up in subjects with SDA found:

• SDA provides sufficient oral functions and comfort and that loss of molars is not a risk factor for
TMD.
• Minor changes in interdental spacing happened shortly after extraction until equilibrium is achieved
and remained stable: The differences in contact relation of the teeth (interdental contact within the
arch and contact of the upper and lower anteriors) are an indication of adaptive migration, which
takes place in the remaining dentition
• Attrition and alveolar bone height don’t differ significantly from complete dental arches.
• The masticatory performance decreases linearly with the mastication platform area, the masticatory
ability remains sufficient as long as the dental arch length comprises the anterior teeth and 3-5 OU, a
so called “premolar dentition”
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It is important to consider age of patient, as molar support should be maintained until 40 or 50 years
of age. For the elderly and older elderly even extreme shortened dental arch can provide adequate but
minimal functional level.

However this concept has its limitations, cases where SDA cannot be applied:
1- Periodontal problems
Natural teeth should be periodontal dx. free and the status should be carefully evaluated. In
case of active periodontal disease, a course of non-surgical periodontal management should be
planned but in case the teeth exhibit extensive attachment loss and mobility then prognosis are
doubtful. Failure to establish stable periodontal health will have negative consequences in the
long run, such as, drifting under occlusal load, loss of alveolar bone and loss of space for
denture teeth in the long term. (Allen, 2008).

2- Intensive occlusal activity (bruxism):

Evidence of traumatic occlusion, fracture of restorations or teeth, mobility of teeth, dental pain
not explained by infection, TSL long term threat that compromise survival of teeth and cause
gradual loss of occluding contacts and occlusal stability, may also contribute to TMD. (Allen,
2008).

3- Tooth structure of remaining dentition (caries, RCT):

Caries must be controlled and the patient should not be prone to recurrent caries
Previous caries management may result in heavily restored teeth which are structurally weak
and the clinician must judge whether heavily restored tooth is capable of withstanding occlusal
loads as part of a shortened dental arch, especially endodontically treated tooth. Ideally, it
would be preferable to provide a group function occlusal scheme with SDA but may not be
possible without extensive reorganization of occlusion. (Allen, 2008).

Other cases include: (Witter, 1999)

◦ Young age,
◦ Unfavourable occlusal relationship of the upper and lower anterior teeth (severe Angle
Class II or Angle Class III)
◦ Pre- existing TMD
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Question 2: How to manage clicking TMJ?

Temporomandibular disorder (TMD) is a collective term embracing a number of clinical problems

that involve the masticatory musculature, the temporomandibular joint and associated structures, or
both.
Royal Collage of surgeon’s guidelines, 2013
o The prevalence may affect up to one third of the population, ranging from 5-50%.
o Most common cause of chronic pain in the orofacial region.
o TMD is considered the 3d most common chronic pain problem after headache and backache.
o Affects female more than male ratio 2:1

Predisposing factors: (Lyons, 2008)

o Systemic factors, such as biochemical susceptibility, stress, anxiety and depression.
o Structural factors, such as some occlusal features, deep overbite, loss of molar teeth, anterior open
bite and joint laxity may be significant to some degree.
Initiating factors: include parafunction (such as bruxism, nail-biting, gum chewing), adverse loading
and trauma.
Perpetuating factors: include behavioural, social and emotional problems.

The signs and symptoms: (RCS guidelines, 2013)

o Pain in TMJs and muscles of mastication, worsened by function
o Muscle and joint tenderness on palpation
o Joint sounds (clicking or crepitus)
o Limitation and incoordination of mandibular movement
o Headaches
o Otalgia = earache
The gold standard for diagnosis is the Research Diagnostic criteria for TMD (RDC/TMD) which
provides a physical diagnosis of the most common TMDs and a measure of the psychosocial disability.

Common diagnosis:
o Affecting the muscles is Myofacial pain w/o limitation of opening.
o Disc displacement with reduction (with clicking)
o Disc displacement without reduction (locking)
o Osteo-arthritis = articular degeneration with pain and crepitus
o Osteo-arthrosis= crepitus without pain

Clicking TMJ: (Gray & Al-Ani, 2013)

 An early or mid opening cycle click is commonly caused by disc displacement. Once the
rotatory phase (which is the first 15-20 mm) is exceeded, translation occurs when the head of
the condyle moves forwards across the intra-articular disc. If the disc is displaced then as
translation commences, the head of the condyle encounters the disc in an unexpected and
displaced position. Friction is built up until the head of the condyle ‘jumps past’ the disc with a
positive audible release of energy, which is the click.
 The closing click tends to be softer than opening click, as it is more of a passive movement
when the disc repositions. Late opening click could be subluxation, when the disc is not
displaced at the commencement of mouth opening, but the click occurs as a result of the
condylar head moving considerably further than the disc and, thereby, attaining a displaced
position
 Early morning click: The click associated with facial arthromyalgia or myofascial pain tends
to be present on waking in the morning for the first hour or so. Thereafter, as the muscles relax,
the disc returns to its normal anatomical and functional position, owing to the elastic pull of the
posterior part of the disc, and the click disappears. May return at times of increased muscle
tension, such as when eating.
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 Click is consistently present throughout movement, this is more indicative of a true internal
derangement in which the disc is consistently displaced. It is important to differentiate
between the two types of clicks on the basis of the patient’s history, as this will directly affect
the treatment plan.

Management of clicking:
o If a patient presents at the surgery with a painless click that is completely symptom free, there is no pain
and there never has been any experience of locking, there may be no need to treat the condition.
o If the click is painful, if there is a tendency to lock or if it is audible to others and socially embarrassing,
then the treatment of choice is an anterior repositioning splint., which is successful in 85% of
patients reported by Davies and Gray, (1997).

Anterior repositioning splint rationale:

When the patient postures forwards onto his/her incisor teeth, the head of the condyle projects
downwards and forwards so that the displaced disc assumes a more normal ‘functional’ relationship
to the head of the condyle. Opening and closing from this position without causing the click thereby
eliminates trauma to the disc and the natural elasticity of the posterior part of the disc gradually
repositions it.
o The splint should be worn 24 hours daily for 12 weeks followed by gradual wearing off period.
o Works well when the patient has click when opening in the vertical dimension.

Management of TMD in general: (RCS guidelines, 2013)

Reversible, which we start with:

 Self-management with an explanation of the diagnosis and its benign, largely non-progressive
nature. (Behavioural therapy):
o Encourage relaxation and to control the amount of the masticatory activity.
o The patients have to pay close attention to the jaw muscle activity, to avoid oral habits and
excessive mandibular movements.
 Physical therapies:
o Feine & Lund, (1997) systematic review and meta- analysis concluded that physiotherapy
has good short-term efficiency, whereas long-term effects are similar to placebo.
o Home exercises and care: Breathing, massage, stretching, relaxation, mobilization and
coordination exercises, moist heat and crytherapy (ice packs). There is some evidence to
suggest that a home exercise programme may be beneficial to some patients.
o Acupuncture: La Touche et al. (2010): systematic review and meta analysis showed that
Acupuncture evidence is limited and show short term benefit for TMD of muscular origin.
o Short wave pulse therapy, ultrasound and soft laser may be helpful, particularly if trauma
has been involved.
o Transcutaneous electrical nerve stimulation (TENS) − has been found to be useful in
some cases.
 Pharmacotherapy: NSAIDS and Benzodiazepines (for relieve of acute phase)
 Occlusal splint therapy:
o Occlusal splints have proven to be helpful in many cases, with good evidence to support the
efficacy of splints for at least partly relieving TMD symptoms
o Soft splint, It may stimulate additional muscle activity not for prolong use.
o Stabilisation splint, Michigan splint is the most widely-used appliance for the treatment of
TMD: For maxilla, Canine guidance, Even point contact on posterior teeth and light contact
anteriorly, Can be hybrid or hard. Tanner splint is the same but used for the mandible,
sometimes for class 3 occlusion
o Anterior repositioning splint: successful in about 85% of patients with clicking .
 Psychological interventions: Hypnosis and relaxation therapy, Zhang et al. (2015): systematic
review and meta analysis revealed limited or no benefit on pain reduction, beneficial effect
maybe on maximum pain and active maximum mouth opening.
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Irreversible:

 Occlusal adjustments: DeBoever et al.( 2008) + Koh & Robinson (2004) review articles
concluded that there is little or no evidence to support occlusal corrections as primary therapy
and is never indicated as prevention.
 Surgery. − options include arthroscopy, with or without joint lavage, and meniscal plication
(means folding). However, surgery is only required in a very small proportion of patients and
only where there is a structural joint disorder.

Outcome assessment for TMD therapy:

Given the biopsychosocial nature of TMD, and dependent on the nature and origin (myogenous or
arthrogenous), there are a number of areas that can valuably be assessed at repeated follow-ups:
Assessment of current symptoms through a repeated history at the review visit.
Objective clinical measurements (for example, jaw opening measurements).
Simple pain scales and multidimensional patient reported outcome measures (PROMs) are
currently under development. (Simple pain intensity from 1-10 or asking patient to mark a
visual analogue).
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Question 3: GIC composition, setting, advantages and disadvantages?

Self-adhesive restorative material first described by Wilson and Kent in 1972.

Composition:
o Powder → A mixture that is fused at high T0 and then cooled and finely ground into powder particle
size ranging from (15-50 micrometres) depending on the application (restorative or luting GIC):
▪ Alkaline calcium fluraaluminosilicate glass + freeze dried polyacrylic acid
▪ Strontium, barium or zinc oxide provide radio-opacity
▪ Tartaric acid: delaying initial setting and then providing rapid onset reaction, thus
giving longer time to manipulate, also increases compressive strength.
o Liquid → water, medium for the reaction and hydration.
▪ Between 11-24% of the set GIC is water
▪ Its critical that that GIC is not dehydrated (by RD isolation or finishing and polishing
without water), if water is lost this leads to excessive shrinkage.
▪ GIC is also damaged if exposed to excess water, calcium and aluminium cations
required for the setting will be eluted, producing weak chalky surface. Therefore the
surface of the GIC restoration should be protected by methacrylate based resin
(bonding agent) or petroleum jelly.

Methods of mixing:
o Manual: powder and liquid ratios measured and mixed manually
o Mechanically mixed: supplied in capsule with the powder and liquid accurately proportioned, when the capsule is
activated the liquid is released into contact with the powder and an amalgamator is used for mixing.

Setting reaction: involves three stages:

o Dissolution: powder and liquid coming together, the acid becomes a solution. Then the H ions are
released from the acid and react with the outer layer of the fluroaluminosilicate glass releasing the
cations (AL, Ca, Na, F), the loss of the ions converts the outer layer of the glass into siliceous gel.
o Gelation phase: the Ca ions are released most rapidly cross-linking with the acid to form salt (Ca
polyacrylate salts). At this stage its very vulnerable to excess water. (Divalent crosslink)
o Hardening phase: it can last up to 7 days, Aluminium forms crosslinking with the acid forming
aluminium polyacrylate salts. Which provide the final strength of the cement (trivalent crosslink).

Fluoride release: F ions are released during the mixing and lies in the matrix and can be release
without affecting the physical properties of the cement, the initial release is high but declines after 3
months, after that it continues slowly for a long period, F can also be taken up by the cement during
topical F treatment acting as a reservoir.

Advantages:
o Tooth coloured
o Bond chemically to tooth and non-precious metal without need of adhesive
o Fluoride release (controversial benefit, no conclusive evidence of anti-cariogenic property, Randell
& Wilson 1999)
o Coefficient of thermal expansion equivalent to tooth
o Biocompatible

Disadvantages:
o Low fracture toughness, compressive and tensile strength
o Some types cant be finished and polished in the same visit
o Some types vulnerable to acid erosion, deterioration at low pH
o Some have low flexural strength and wear resistance
o Sensitivity to moisture during setting
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Question 4: List composite types and compare tensile and compressive strength of each?

Composite components:
o Resin→ monomers Bis-GMA, UDMA
o Viscosity controller→ TEGDMA low viscosity monomer to dilute the composite
o Fillers→ quartz, silica, glass particles
o Coupling agent → silane
o Initiators→ tertiary amines, toluidine, camphorquinone
o Inhibitor → hydroquinone, to increase shelf life
o Barium for radiopaque property

Types of composite differ in properties according to the type, size, and content of filler particles:
According to filler particle size:
o Traditional or Macrofilled: quartz (10-20 micrometer) 75-80% by weight
o Microfilled: colloidal (0.01-0.05 micrometer) 40-50 % by weight, highly polished and aesthetic
(translucency)
o Hybrids: large filler particles (15-20 micrometers) + small (0.01-0.05) , 75-80% by weight, strength
and physical properties
o Nano- composites: (100 nanometer) 80-87% by weight

Materials:
o Flow able composites: less filled (40%) with more resin→ higher polymerization shrinkage, inferior
physical properties
o Packable composites: high filler amount, less resin → less polymerization shrinkage (1.7-2.5%
shrinkage)
o Resin luting cements: adhesive cements under ceramic restorations, indirect composites (Variolink,
Calibra, Panavia, Rely-X)
o Core build-up composites: dual cure, self cure, (Paracore, Ti-core)

Physical properties:

o Compressive strength: is a measure, in which a disc of the material is subjected to a compressive

load. It is commonly used test for brittle materials.
o Tensile strength: measured when a sample is stretched in a uniaxial direction under constant strain
rate.

Material Compressive strength MPa Tensile strength MPa

Enamel 384 10
Dentin 297 52
Macrofilled 250-300 50-65
Microfilled 250-300 30-50
Hybrid 300-350 70-90

o Although they have similar compressive strength, the tensile strengths are different.
o The hybrid has superior physical properties and good aesthetics.
o The microfilled except for compressive strength, all other physical and mechanical properties are
inferior to other types, however, it provides smooth, polished surface desired for aesthetics.
o Macrofilled physical properties are intermediate, but as a result of wear from brushing and
mastication, it develops a rough surface, which has tendency to discolour.
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Question 5: Explain how to diagnose caries, early carious lesion and root caries management,
and explain fluoride action and products?

Caries is a multifactorial disease process that it dynamic in nature affecting tooth structure, the
necessary elements are the bacteria within the biofilm that metabolize dietary sugars producing
acids, which over time lead to demineralization of the tooth structure. {Venn diagram}

The Biofilm:
o Forms on any solid surface exposed to appropriate amounts of water and nutrient. The dental tissues -
enamel, dentin, and cementum—are coated by a pellicle to which the microbial cells attach.
o The primary colonizers and secondary organisms generate a matrix of exopolymer within which cells grow
o A community of organisms is formed rather than a haphazard collection of bacteria
o The community has a collective physiology which can solve the specific physicochemical problems posed by
the environment at the site
o Always metabolically active, causing fluctuations in pH
o These fluctuations may cause a loss of mineral from the tooth when the pH is dropping or a gain of mineral
when the pH is increasing
o The cumulative result of these de- and re-mineralization processes may be a net loss of mineral, leading to
dissolution of the dental hard tissues and the formation of a caries lesion (Stephans curve)
o The biofilm tends to form and mature in certain locations on the tooth, notably the occlusal surface, especially
during eruption, the approximal surface cervical to the contact point, and along the gingival margin
• Lactobacilli were identified as major acid producers and then, from the beginning of the 1960s,
much focus was on mutans streptococci. , both prefer to grow and metabolize at low pH
(acidogenic and aciduric)
• “Ecological plaque hypothesis” This condition favors the proliferation of aciduric bacteria such as S.M
and L.B, and others.

Carious process:
o Under physiological conditions (pH 7.4) saliva and the oral fluids are super-saturated with respect to
hydroxyapatite and fluroapatite
o As pH is lowered in the oral fluids, the supersaturation with respect to hydroxyapatite is reduced and at
critical pH (5.5) the fluids become saturated with respect to hydroxyapatite
o Fluroapatite is less soluble than is hydroxyapatite, and therefore remains supersaturated in oral fluids
o Subsurface hydroxyapatite is dissolved, while fluorhydroxyapatite is formed in the surface layers of enamel
o However, the concurrent supersaturation with respect to fluroapatite is responsible for the maintenance and
integrity of the surface layer
o The solubility of apatite increases by a factor of 10 with a drop of each single pH unit
o The bacteria penetrate into the tissues and in addition to acid production they also start proteolytic activity
once they reach dentine
o This leads to the degradation of partly demineralised collegen and while probing this is the soft, sticky,
yellowish/brownish carious dentine

White spot lesion:

o Why the white-spot lesion looks white and why a dentist, looking at a clean tooth surface, can, using
vision and a three-in-one syringe, determine the depth of penetration of the lesion→ because of the The
porosity of the subsurface lesion
o The lesion that is visible only on a dry tooth surface is probably in the outer enamel, whereas a lesion
visible on a wet tooth surface has penetrated most of the way through the enamel and maybe into the
dentin:
• Relative refractive indices of enamel, water, and air
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• Enamel has a refractive index of 1.62
• In the subsurface lesion, the pores are filled with a watery refractive index of 1.33
• The difference in refractive index between the water and the enamel affects the light scattering
and makes the lesion look opaque
• If the surface is then dried, air, with a refractive index of 1.0, replaces the water
• The difference in refractive index between the air and the enamel is now greater than that
between the water and the enamel
• This means that the lesion becomes more obvious, and an earlier lesion can be detected.

o White spot lesion contains more fluoride than the surrounding sound enamel
o The surface layer exerts a protective effect to prevent further dissolution of the lesion body as long as the pH
fluctuations are in the range of 4-5.6
o When about 30-40% of the mineral in the enamel lesion is lost, it becomes so porous and fragile that it may
easily break apart and a cavity forms
o Once a lesion has become inactive (or arrested) its appearance cannot be changed unless the surface is
mechanically polished or ground or by stripping a layer off it with a strong acid
o Only when crystals are partly dissolved are they able, with time, to allow calcium and phosphate ions to
redeposit on the partly dissolved crystal surfaces
o Remineralization of enamel subsurface caries lesions requires that calcium and phosphate ions are able to
diffuse into the porous subsurface enamel usually through the relatively intact surface zone
o Remineralization of dental lesions requires the presence of partially demineralized apatite crystals that can
grow in size as a result of exposure to solutions supersaturated with respect to apatite
o The formation of entirely new crystals in a subsurface lesion is not likely
So, what is dealt with clinically when talking about remineralization is predominantly surface changes,
which are a combination of abrasion of the porous enamel, and a slow re-deposition of mineral in and
onto the partly dissolved crystals. The surface layer of the lesion protects the underlying lesion body
not only from demineralization, but also from remineralization.

Histology of white spot lesion:

• White spot lesion on a smooth surface has been sectioned longitudinally, then placed in water and
viewed in polarized light:
Surface Zone (1% demineralized)
Body of the lesion (porous >5%)
• These zone are only visible when the ground sections are examined in quinoline
Dark Zone (2-4% porosity), when placed in quinoline (big molecule), cannot penetrate all micropores (uneven
holes) which remain filled with air hence the “Dark appearance”
Translucent Zone (pores slightly more than 1%)
Histology of dentinal caries:
• Zone of destruction:
Most superficial part of the dentine;
Decomposed by the action of acids and enzymes.
• Zone of penetration:
Tubular invasion of bacteria.
• Demineralized dentine:
Does not yet contain bacteria
• Dead tracts:
Rapid lesion progression → odontoblast processes have been destroyed → no tubular sclerosis.
• Reparative dentine:
Released by new odontoblasts or odontoblast-like cells

Root caries:
• Root caries is similar to enamel caries in being a subsurface demineralization
• But, the surface may appear softened at an early stage. Bacteria penetrate at an earlier stage
• Interestingly, although these lesions may appear rather extensive, they are seldom more than
0.5 to 1 mm deep.
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Clinical examination of caries (smooth surface caries, pit and fissure caries, approximal
caries): Diagnosis: implies detecting a caries lesion, estimating its depth and degree of
demineralization, and making a decision about its activity
• Visual examination: (both wet and dry to detect white spot lesion, which are clearer in dry tooth
rather than wet because of the refractory index difference between air and enamel (air=1,
enamel=1.66, water=1.33). Based on the international Caries Detection and Assessment System
(ICDAS II) this system characterizes the visual appearance of the lesion with their histological depth.
• Visual and tactile: using floss or probe to remove biofilm, assess fit of restoration or any loss of
surface integrity, however the probe must not be used with pressure to detect stickiness as this can
damage the early lesion.
• Caries detection devices:
o Laser florescence device (DIAGNOdent), which detect fluorescence from bacterial
Porphyrins. Wavelength is 655nm red light range, needs carful cleaning of tooth surface as
stains and calculus can provide false positives, and when used around metallic restorations.
Better used for occlusal lesions (pit and fissure).
o Transillumination (FiberObticTransillimination), carious lesion have lower index of light
transmission thus appear darker. Can be useful for proximal lesions and overlap teeth.
o Caries detection dye: 1%acid red solution in propylene glycol.
• Intraoral radiographs (BW and PA): remains the examination of choice for evaluation of
restoration margins and caries adjacent to restoration, 50 % loss of mineral to be visible in
radiograph. (Approximal caries and hidden occlusal caries)
• Temporary separation and impression: use of elastic bands for 24-48 h, and impression to record
cavitation. (Approximal caries)

Caries Risk assessment: is a prediction as to whether a patient is likely to develop new caries in the
future. For high caries risk patient, restoration of caries teeth is not the solution. First assessment to
establish main risk factors and treatment plan to address them, once the preventive approach has
been initiated, stabilization of active caries is required and elimination of plaque retentive factors.
Reassessment (6-12 months) of the caries risk is required over a period of time before advanced
operative treatment is considered.

What are the caries risk factors and how to assess them?
o Social deprivation: deriving from overcrowding, male unemployment, low social class and no car.
o Past caries experience: strong predictor of future caries, assessed in history taking and charts.
(DMFT, DMFTs)
o Oral hygiene: can be assessed by Silness and Loe plaque index buccal and labial surfaces of
undisclosed key teeth (molar, premolar and incisor): (screening tool) or full mouth plaque scores
o 0= No plaque
o 1= plaque visible on probe
o 2= plaque visible with the naked eye
o 3= plaque visible all around tooth
o Diet: by pt. recollection and appropriate questioning or a diet diary of three consecutive days. And
appropriate analysis and advice should be given in terms of frequency and sugar content.
o Fluoride: information of use of fluoride should be gathered in order to see if the concentrations are
enough or require more interventions.
▪ Toothpaste→ 1400 ppm sodium F, or sodium mono-fluoro-phosphate.
▪ High dose tooth paste Duraphat→ 2800 ppm- 5000ppm (>16ys)
▪ Duraphat varnish for less than 10 yrs → 2.26% sodium fluoride
▪ APF (acidulated phosphate F)gel → 1.23 %
▪ Mouthwashes→ daily 0.05%, weekly 0.2 % sodium fluoride
❖ Cochrane SR by Marinho et al. 2016, evaluating the effect of topical F for
preventing dental caries, showed that supervised daily or weekly F MW result on
average in 23% fewer DMF permanent tooth surfaces. However no info. On side
effects.
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❖ Cochrane SR by Walsh et al. , F toothpaste of 1000ppm and above result in
prevention fraction of DMF of 24%, however the use of it in children should take into
account the risk of fluorosis.
o Saliva: conditions dry mouth or medications (antihypertensive, diuretics, antidepressants,
antipsychotics, antispasmodics and some antihistamines), other causes autoimmune dx. Sjogren’s
syndrome, diabetes, radiotherapy to head and neck, recreational drugs, caffeine, alcohol and
amphetamines.
o Examination can be obvious→ mirror sticks to the oral mucosa
o Measures of quantity:
▪ Unstimulated (normal 0.3 ml/min, dry mouth <0.1).
▪ Stimulated (normal 1.5ml/min, dry mouth <0.5 female and 0.7 male)
o Saliva microbiology: (M.S. and L. B. CRT bacteria counts kit) chair side mixed saliva
collected in culture plate and incubated at 37o for 48 h and the no. of colonies forming units
(CFUs) if the counts are higher than 10% the pt. is high risk
o Saliva buffering capacity: measured using Dentobuff buffer kit
o Measure lactic acid (pH level) using Clinpro Cario Diagnosis, using impression material for
specific site (sucrose converts into lactic acid→ converts to Pyruvate → which binds to stain
reaction (blue colour), or swap plaque from tongue.
Cariogram: a computer based caries risk model collecting data from clinical, radiographic and
saliva tests and give a score from 0-3 or 0-2. Which gives an indication of future caries risk as
“chance to avoid”.

How to manage early white spot lesion? (White spot lesion developed in 4 weeks time if plaque
is not removed and reminralised in 4 weeks with brushing, fluoride and M.W:
o Non-invasive treatments: start with prevention and improve oral hygiene, professional cleaning, and
fluoride, improve plaque reduction.
o Monitor the lesion:
o If it is still there → micro-invasive treatments: sealing and resin infiltration,
▪ Sealing is performed to prevent dental caries in the pits and fissures on the occlusal or
pitted tooth surfaces: For (carious) surfaces, clinicians can also apply sealants
therapeutically
▪ Resin to reinforce the lesion (resin infiltration) is the fact that the pseudo-intact
surface layer present in non-cavitated proximal lesions needs to be removed prior to
infiltration via acid-etching, using hydrochloric instead of phosphoric acid, uses
light-curable low-viscosity resins (infiltrants), which are soaked up into the porous
enamel lesion body
❖ A Cochrane SR by Dorri et al. 2015, evaluating the effect of micro-invasive tx. For
proximal carious lesions, available evidence shows that they arrest non-cavitated
enamel and initial dentinal lesions more effectively than non-invasive tx. (varnish) or
advice (floss).

o If the lesion broken down (deep carious lesion) → Conventional invasive treatment usually
involves the use of rotary burs, alone or in conjunction with metal hand instruments (e.g.
excavators), to remove carious (i.e. infected and demineralised) dentine and then place a
restoration
❖ A Cochrane SR by Ricketts et al. 2013, Stepwise and partial excavation reduced the
incidence of pulp exposure in symptomless, vital, carious primary as well as permanent
teeth. Therefore these techniques show clinical advantage over complete caries removal
in the management of dentinal caries.

Mechanism of Fluoride action:

• Effect during tooth formation.: high affinity to Ca in hydroxyapatite, harder enamel more resistant
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• Inhibition of plaque bacteria at pH 7.0 F ions precluded from entering bacteria at pH 5.0 F exists as HF which
interferes with bacterial acid production by inhibition of enolase. (Interfere with bacteria metabolism)
• Affects crown morphology making pits & fissures shallower.
• Inhibits demineralization when in solution.
• Enhances remineralisation by forming Fluor-apatite.( reservoir of F)
• Critical pH is 5.5 for apatite.
• At pH 5.0 apatite demineralises. And at pH 7.0 apatite remineralises.
• If F is present fluor-apatite forms→ Fluor-apatite is resistant to acid attack until the pH drops to 3.5

Key points:
• Difficult to explain 50% reductions→ Impossible to get complete substitution of OH for F ions
(enamel F would = 3.7%).
• It is the activity of the fluoride ion in the oral fluid that is of most importance in reducing enamel
solubility rather than having a high content of fluoride in surface enamel.
• A constant supply of low levels of intra-oral fluoride, particularly at the saliva/plaque/enamel
interface, is of most benefit in preventing dental caries.

Fluoride products: (systemic or topical)

• Water: 5.5 million in UK (7%), 1.0ppm F is optimum level, caries reduction by 50%, most cost
effective.
• Salt, milk:
o Salt -50% reductions in Switzerland & Hungary.
o Milk -15-65% reductions.
o Orange juice -25% reductions.
o Mineral Water -46% reductions in Bulgaria

• Supplements: Results of caries reductions vary 20-80%, Poor compliance 3-5%, fluorosis?, dose variation worldwide.
o No application as a public health measure.
o 0.5mg/day from 3yrs for at risk patients.
o Not to be used before 3 years of age unless prescribed by a dentist.

• Toothpastes:
o They usually contain 1000 or 1450ppm F. caries reduction by 24%
o NaF or Na monflourophosphate or a combination of both.
o Child formulations 250-500ppm F (under age of 6 to minimize F ingestion and risk of fluorosis)
o High F toothpastes by prescription only: 2800 ppm, 5000ppm: 76% caries reduction for pt. prone to root caries, dry
mouth, high sugar diet, elderly
• Rinses: Daily 0.05% NaF (225 ppm F), Weekly 0.20 % NaF (900 ppm F)
o 20-50% Caries Reductions
• Professional Gels: 1.23% APF Gel (12,300 ppm F), Biannual applications or quarterly for rampant
caries cases, 26% caries reduction: APF Safety Recommendations:
• No more than 2ml per tray.
• Sit patient upright with head inclined forward.
• Use a saliva ejector.
• Instruct the patient to spit out for 30 seconds after the procedure (usually 1 or 4 minutes).
• Do not use for children under 6yrs.

• Self application gels: Neutral NaF 5000 ppm F. (APF 5000 ppm F, SnF2 1000 ppm F)
o Trays 36.1% caries reductions
o Brush-on 24.0% reduction
 13
• Varnishes: Duraphat 2.26% NaF (22,600 ppm F), Fluor Protector 0.9% wt fluorsilane
o 33% Caries Reductions
o Biannual applications or quarterly for rampant caries cases.
o Quick and easy to use.
o Contraindicated for severe asthma
• Devices

Fluoride toxicity:
Early symptoms: Nausea, Vomiting, Hyper salivation, Abdominal Pain (HF, ulcers), Diarrhea
Late symptoms: Convulsions (fall in plasma Ca), Cardiac Failure, Respiratory failure, Death
Treatment:
1) Induce vomiting (to remove F).
2) Give milk or 1% calcium gluconate orally to slow F absorption.
3) Advise hospital of acute F poisoning.

The Probably Toxic Dose (PTD): was defined by Whitford as the minimum amount of fluoride
ingestion that requires action, and is 5mg/Kg body weight. The PTD for a 5yr old child (average
weight=20Kg) is 100mg fluoride.

Risk of fluorosis in aesthetic area: For permanent central incisors the period of maximum risk is a
4 month period from: 22-26 months. Exposure prior to this carries less risk than continual exposure
for up to 36 month.
Risk in general: below age of 6

Types of dental fluorosis: (mild, moderate, severe)

• Demarcated
• Diffuse
• Hypolpastic
• Combinations

Skeletal: Can be crippling. Fusion of intervertebral discs/ligaments

Osteoporosis: Head of femur (Elderley and PM women)
Kidneys: Renal Disease & Renal Failure

American Academy of Pediatrics 1986

For optimal dental health the total daily intake of F should be: 0.05-0.07 mgF/Kg Body Wt
To avoid the risk of dental fluorosis should not exceed a daily level of: 0.10 mgF/Kg Body Wt

Treatment options for fluorosis:

• Microabrasion: technique: Aim of all is to remove surface layer of enamel with a combination of
erosion and abrasion (100μm) to improve aesthetics:
o Clean teeth to be treated with water and pumice
 14
o Isolation with rubber dam
o Vaseline below rubber dam if using 18% HCL
o Mix 37% phosphoric acid gel / liquid with pumice
o Apply with rubber cup / flat plastic 5-10sec
o Wash of with water
o Repeat up to 10 times
o Polish with super fine Soflex disc
o Polish with fluoridated tooth-paste
o Review in 1 month
Supporting evidence:
o Brown stains almost 100% improvement
o White stains 60-100% improvement (Welbury and Shaw 1990)
o Optical properties of enamel are altered →Combined abrasion and erosion results in a densely
compacted prism-free layer.(Olin et al 1989)
o Reflection and refraction of light altered –camouflage of underlying stain.(Elkhazindar and
Welbury 2000)

• Composite veneers
• Porcelien veneers
• Crowns (all ceramic, dentin bonded, PFM)

Question 6: Define dentine hypersensitivity, prevalence in population and perio. Patients

explain the difference and management?

Defined as pain arising from exposed dentin typically in response to thermal, chemical, tactile or
 15
osmotic stimuli. that cannot be explained as arising from any other forms of dental defect or
pathology (Addy & Urquart 1992).Can be dull or sharp, vague or specific, intermittent or constant.

Dentin exposure can be as a result of one or combination of the following factors:

o Enamel or cementum removed as result of attrition, erosion and abrasion.
o In some patients the cementum and enamel don’t meet leaving an area of exposed dentin
Regardless to the cause, the patent dentinal tubules are open which provide direct link between the
environment and the pulp. Once sensitivity has established the pulp may become irreversibly
sensitive.

Theories of dentinal sensitivity:

1. Odontoblastic process theory: exposed process on the surface are excited by stimuli
(chemical/mechanical) → releasing neurotransmitters → impulses travel toward the nerve endings
(to date no neurotransmitters have been found)
2. Neural theory: the stimuli (thermal/mechanical) directly affect the nerve endings within the tubules
(direct communication with the fibers)→ supported by presence of unmyelinaed nerve fibers in the
outer layer of root dentine + putative neurogenic polypeptide. (Little solid evidence)
3. Hydrodynamic theory: the most widely accepted proposed by Brannstrom et al. 1972: fluids in the
tubules are disturbed by stimuli (T, physical, osmotic pressure) → movements stimulate baroreceptor
leading to neural discharge.

Epidemiology:
o Common problem→ incidence of between 4 to 74 %, discrepancy is due to:
▪ Different methods used to diagnose the condition,
▪ Variation in the consumption of erosive foods and drinks. (Wazani et al 2012): prevelance of sensitivity
in tooth wear cases up to 40%).
▪ The type of setting where the study was carried out. Studies carried out in a periodontal specialist clinic
tend to report higher prevalence values of sensitivity ranging from 60.3 to 98.
▪ Variation in methods of data collection, and the actual diagnosis as having cervical dentin
hypersensitivity,
o In most population it is between 10 -30 %,
o In dental practice setting Rees et al. 2000 reported a lower value of 3.8%. Lower percentages could
be due to study was based on clinical examination and not self-reported questionnaire.
o Rees & Addy, 2002 cross-sectional study of dentine hypersensitivity, reported a value of 4.1% range
of (1.2 - 18%in practices), commonest tooth first premolar, commonest initiator is cold (55%), and in
higher socioeconomic classes.
o Upper premolars followed by upper first molars are most commonly affected. The incisors →least.
o Higher incidence in females not statically significant, age range 20- 40, peak at the end of 3rd decade
and decrease in 4th and 5th decade, may be due to decrease in permeability of dentine with aging
(sclerosis and secondary dentin) and long term use of F tooth paste
Prevalence of sensitivity in periodontal patients, and why is it different?
o Periodontal pts. with recession and smokers with periodontitis show highest incidence (72.5% and
98% (Chabanski et al.1997).
o Rees et al. 2003, Hong Kong hospital periodontology clinic, reported 67.7%, the commonest teeth
are the lower incisor (as the single rooted teeth respond better to NSPT, and retained for longer +
crucial aesthetic position) and the commonest initiator is cold drinks.
o Reasons for that are:
• As part of the periodontal disease process the root surface may become exposed.
• Dababneh et al. 1999, suggested DH in perio. Pt. possibly related to the bacterial penetration of the
dentinal tubules.
• The greater risk of root exposure as a result of periodontal attachment loss and gingival recession
following periodontal treatment, vigorous traumatic tooth brushing (76% of sensitive teeth had recession,
Rees et al. 2003)
 16
Treatment strategies:

1. Nerve desensitization: Potassium nitrate, efficiency demonstrated by Tarbet et al. 1980-1982 at a

concentration of 5% in a low abrasive toothpaste is able to desensitize dentine for up to 4 weeks.
Also as bioadhesive gels at 5% and 10% also effective.
o Mechanism of action: largely unknown, likely explanation is that potassium reduces sensory nerve activity
due to the depolarizing activity of the K ion. {this has not been confirmed in intact human teeth}
o Good evidence support to its benefit

2. Anti-inflammatory agent: corticosteroids, through inducing mineralization leading to tubule

occlusion, however not validated and questioned
3. Covering or plugging the DT:
• Calcium hydroxide via occlusion of DT through the binding of loose protein radicals by Ca ions
and increasing mineralization. Immediately effective but rapidly diminishes requiring multiple
application + irritation of gingival tissues.
• Casein phosphopeptides, new product not yet proven
• Sodium fluoride, due to increase resistant to acid decalcification + precipitations in the DT.
Mechanically blocking them /within them blocking the transmission of stimuli (Tal et al. 1976 )
• Sodium monofluorophosphate, unclear MOA, occluding effect not permanent
• Stannous fluoride, aqueous or gel, MOA through the induction of high mineral content creating
calcific barrier blocking the DT
• Fluoride iontophoresis, influencing ionic motion by electric current → immediate reduction but
gradually return over 6 months
• Formaldehyde or glutaraldehyde, MOA ability to precipitate salivary proteins in DT,
questioned effect and should be used with extreme caution to ensure they don’t contact gingival
tissues (as they are tissue fixatives)
4- Dentine sealers:
• Resins and adhesives: issues when the adhesive breaks away, for cases with specific and
localised DH
5- Lasers:
• Nd:YAG have been studied MOA ability to occlude the DT. Used with sodium F varnish show
up to 90% of the DT occluded
• CO2 laser and stannous F gel effective for up to 6 months, still require investigations before
being acceptable
6- Combination: 5% potassium nitrate: fluoride dentifrices (safe and effective)
7- Restorative materials: composite or GIC, last resort if not responding to other less invasive Tx
8- Periodontal surgery: lateral sliding graft, free gingival graft, C.T graft an coronal repositioned
• Cover exposed DT, Not predictable in terms of root coverage
• Not predictable for managing sensitivity

Hypersensitivity and plaque: accumulation on root surface → demineralization of tooth structures

→ patency of DT orifices. Pts with good OH reported less likely to have DH (however it is
controversial, many pts have gingival recession with minimum plaque yet complain of sensitivity.
Most effective Tx.:
• Daily plaque removal → to allow remineralisation from salivary minerals
• Use of desensitizing toothpaste

(Bartold, 2006)
Question 7: Define Overdenture and differentiate from Onlay denture in terms of indications,
advantages and disadvantages of overdenture, what abutment factors to consider when
planning overdenture?
 17
The roots of teeth have been used to support dentures since 1856. In 1958, Miller reintroduced the
concept of using teeth to stabilize complete dentures.
Overdenture is a complete or partial denture fabricated over one or more retained natural teeth or
roots in a dental arch and the residual ridge (Lord and Teel, 1969). Fully extended flanges for border
seal retention.

Onlay dentures extends over the incisal or occlusal surfaces of worn abutment teeth with tooth-
coloured acrylic resin and forms a “butt joint” on the labial or buccal surface, it is not recommended
for use if the resin/tooth junction is visible. Less bulky. Carful design is required as they rely on the
remaining teeth for retention.

Overlay denture is, laminates the labial surfaces of worn teeth with tooth-coloured acrylic resin,
which is usually supported by a metal framework or polymeric denture base material. Require
preparation to the gingival margin if the path of insertion is not suitable.

There are two modifications to the above definition:

1. A removable partial overdenture: consisting of conventional tooth support and covering one or more
supporting teeth roots.
2. Completely buried roots or implants may be retained within the bone and a complete denture made
over these.

Advantages:
▪ Functional: retention, resistance and stability.
o Support from the remaining roots helps to protect the residual ridge from force placed on the
denture.
o Minimizing horizontal forces on the abutments: by reduction of crown length, (more
favourable C:R ratio for periodontal compromised teeth.
o The retained roots also offer assistance in stabilizing the denture as it resists lateral
displacing forces.
o Correction of occlusion and aesthetics: when the crowns of the remaining teeth are not ideal,
removal of the crown provides freedom in artificial teeth arrangement.
o Retention provided with or without incorporating of precision attachments.
▪ Physiological:
o The preservation of the proprioceptive mechanisms associated with the periodontal
membrane of natural teeth→ retain some of the ability to be aware of occlusal contact and be
able to control the force of occlusion
▪ Grossman et al. (1965) claimed to show that the natural anterior teeth exhibit more
sensitivity and discrimination than the posterior teeth and therefore give more discreet
sensory input.
o Preservation of ridge form, particularly important in anterior mandible.
▪ (Crum and Rooney, 1975,1978). 5-year Research on the patterns of alveolar bone
loss in patients with mandibular overdentures and in those with conventional dentures
suggests that use of the overdenture preserves alveolar bone especially in the area of
the retained teeth. (50% of bone loss occurred during the first year)
 18

▪ Psychological: to avoid complete loss of teeth and its effect on pts morale

Disadvantages/ Complications:
▪ Recurrence of caries (Hussey & Linden 1986: 27% developed caries in 2years)
▪ Periodontal disease. Attachment loss shown to occur in 35% of overdenture patients
▪ Veneer fracture (Woodley et al 1996: 47% of failures were due to fractures)
▪ Patient dissatisfaction, although a study by (Ettinger & Jakobsen 1997) reported;
o Out of 101 patients: 62 of them were satisfied with their dentures; 33 were satisfied, but
felt they had some faults.
o Only 6 were unhappy about wearing the overdentures.
o The average length of time the dentures worn was 6.9 years, (1-15 yrs range)
o The most frequent complaints were loss of retention (65.4%) and discomfort (62.2%)
of the mandibular dentures.
▪ Endodontic problems: (Ettinger & Qian, 2004):
o 12.9% of endo. Treated abutments had post-procedural problems.,
o Most common problem→ periapical lesion due to recurrent caries and leakage (37%),
o 2nd most common is VRF (30.9%)
o 3rd most common is, vital tooth lost vitality (19.8%)
o Since applying a three step bonding agent to vital root faces (yearly) no further losses in
vitality)
▪ Most losses are associated with poor oral hygiene and inadequate follow-up care.
▪ Poor aesthetics, inadequate retention, lack of stability, discomfort and breakage.

Indication:
1. Arches requiring prostheses where only a few retainable teeth are present. Can be for only one or
two teeth, teeth at gingival level.
2. Patients whose treatment plan indicates extraction of all teeth (easier to incorporate further loss of
teeth) present because they are badly broken down or periodontally involved (not grade III mobility).
3. Patients with poor prognosis for complete dentures, such as those with malrelated ridges,
unfavourable tongue positions or muscle attachments. (Attachments can be incorporated)
4. Where normal reconstruction of the dentition cannot be supported financially.
Contraindicated:
1. Where another method gives superior results-such as (RPD or FPD)
2. Debilitating medical or psychiatric disorders, which rule out essential clinical procedures and
maintenance. (poor oral hygiene, poorly motivated pt.)
3. Inadequate interarch space

Abutment selection: All potential abutment teeth should be evaluated carefully from the viewpoints of:
(a) periodontal status; (b) caries activity; (c) potential for endodontic treatment and (d) positional
considerations.
 19
▪ It is best to select abutments that are in an acceptable state of periodontal health initially, but
often it is necessary to use teeth that are less than ideal. Prospective abutments should have minimal
mobility, have adequate bone support, and be amenable to any indicated perio Tx.
▪ Teeth with minimal or no caries involvement should be selected for abutments. (caries activity)
▪ Endodontic treatment is recommended for overdenture abutments, Endodontic evaluation of
clinical but also a radiographic examination.
▪ For ideal stress distribution, maximal stability and support, the abutments should be well distributed
in the arch.
▪ The teeth most commonly used as abutments for overdentures are canines and premolars.

There are several techniques involved in the preparation of teeth to serve as abutments for the
overdenture (Kotwal, 1977) included in these are:
▪ Simple tooth modification and reduction: remaining teeth are merely reshaped to eliminate undercuts and then
reduced in vertical height if necessary to create more interridge space for the overdenture. The vital pulps must be
receded sufficiently so that the reduced teeth will not be sensitive.
▪ Tooth reduction and cast coping: This is necessary because of sensitivity or as a caries control (they do not
prevent caries), protect weakened tooth from fracture, particularly in the maxilla

Endodontic therapy in the following three techniques facilitates the development of more favorable
clinical crown-root ratios, a better aesthetic result and permits use of tilted or malposed abutment teeth,
hemisected or root-amputated molar teeth.
▪ Endodontic therapy with amalgam plug
▪ Endodontic therapy with cast coping
▪ Endodontic therapy and cast coping utilizing some form of attachment.: This approach is reserved
for the situation in which not only stability is desired but a significant improvement in retention as
well. Because of the added time, cost and risks, this procedure should be reserved for patients with a
favorable prognosis. The abutment teeth need adequate bone support because of the added stress that
the attachment brings to the tooth. Some of the attachments available for use are the Gerber, Dalbo,
Ceka, Zest, Quinlivan and bar attachments.

(Henking, 1982)

Preventing Mechanical Failures

▪ Minimal 2-3mm thickness of acrylic on occlusal surfaces
▪ Provision of metal backings (half backings)
▪ Mechanical retention
▪ Chemical retention (4META)

Follow-up and maintenance

▪ Oral Hygiene needs to be excellent.
▪ Daily application of fluoride gel under the appliance recommended reducing risk of root caries
(Toolson & Taylor 1989, Ettinger & Jakobsen 1997). Compliance can be an issue.
▪ Success is associated with a professional periodontal maintenance programme.

Long-term follow-up and outcome of overdentures:

❖ Toolson and Taylor 1989, 10-year report of 28 overdenture pts. (original no. 89):
 20
o 11 abutment teeth extracted (7 due to caries, 4 perio)
o Caries were found in patients not receiving regular fluoride solution
o Most of the abutments have progressively lost attached tissues other perio. Indices remained
fairly stable.
❖ Ettinger, 1988, 12-year prospective of 254 pts. (71% recall rate):
o Rate of tooth loss of OD abutments was 4.2%
o Most common cause is periodontal dx. (35.7%), 2nd is caries (21.4%)
o Loss of coronal seal and periapical pathosis through RCT (14.3%)
o Vital tooth periapical pathosis (3.6%)
o Most of the failure could have been prevented by adequate OH and recall, since the patients who
had the abutment failure had poor OH due to older age and inability to clean teeth adequately.

❖ Ettinger, 2004, continuation of the 1988 study, up to 22-year prospective cohort report of 273 pts.
o Survival of abutments was 80%, 20% rate of tooth loss
o Most common cause was periodontal dx. (29.3%), followed by caries (16.5%)
o Subjects who lost teeth were more likely to have medical problems, less likely to use fluoride
daily and less likely to return to recall visits.
o Vertical root fractures 22 cases, revealed the maxillary OD opposed by natural teeth were more
likely to fracture.
❖ Ettinger and Qian, 2014, incidence of AL of canines in 53 OD pts. Over 3 recalls in 42months:
o Greatest amount of AL was mid- buccal (5.43 mm) over 3 years
o AL was greater in the mandible canines, could be due to greater amount of movement esp. B-L
direction (rocking)

Question 8: Define Biofilm and mechanism of formation in endo. And how can root canals get
infected?
 21
Biofilms are highly organized multicellular, multi-species structures that collaborate collectively to
harvest nutrients, and display sensing and survival tactics. Features:
• Colonizing species act together to optimize the utilization of local resources
• Intercellular communication. Cells release specific signal molecules into the environment and,
through diffusion or convective distribution and detection by other cells, they communicate when
they have reached a critical cell density
• The collective population co-ordinates efforts in nutritional utilization, virulence expression, and
various other community functions.
• The extracellular matrix develops as a co-ordinated affair, allowing fluids to circulate and an
exchange of cellular components and nutrients amongst the microbial community.
(Figdor & Gulabivala, 2011)
Micro-organisms protected in biofilms are greater than 1000 times more resistant to biocides as the
same organisms in planktonic form. (Wilson et al. 1996) (Nair, 2006)

Formation of plaque biofilm:

1. Dental pellicle formation (acquired pellicle); Thin acellular surface film:

• First layer forms in < 5 seconds
• Low mol. wt proteins laid down first
• Pellicle layer matures over days
• Mature pellicle is (0.1-3.0) μm thick with surface and subsurface layers
• Made mainly of salivary proteins

2. Transportation of planktonic bacteria to the pellicle-coated tooth surface

(Within 2 hours of pellicle formation)
3- Formation of reversible early adhesion of bacteria to pellicle-coated surface.
• This is by weak physicochemical interaction
• These weak adhesion, facilitate later strong/specific adhesion
4- Stronger adhesion between bacterial adhesions and complementary receptors in the pellicle
• Local modification occur; (local O₂ tension, PH, new exposing receptors on surface for
adhesion, making/breakdown of nutrients)
• These facilitate latecomers
• Early colonizers are streptococci sanguinis, strp. oralis, strp. Mitis
5- Adhesion of latecomers with early-attached bacteria
• Specific receptor-adhesion interactions:
Specific protein on one bacteria interact with surface bacteria carbohydrate of another
i.e coaggregation
6. Multiplication of attached bacteria and formation of extracellular polysaccharides
(Sticky, adhesive properties)
• Thus, formation of organized mixed culture biofilm, where microbes modify the environment to suit
their interest (multiplication/growth)
7- Detachment of bacteria by means of enzymes:
• Enzymes hydrolyze the specific adhesion, thus allowing the cells to colonize other sites

Apical periodontitis; is caused by habitat adapted poly-microbial infection of the pulp canal system
by selective oral microorganisms that have breached the enamel, invaded dentine, overwhelmed the
immune response of the pulp and settled in the remaining necrotic tissue.
The microbial flora of root canals in primary infections is dominated by a limited number of obligate
anaerobic microbial species with fastidious environmental and nutritional requirements, i.e. biological
selection has driven the type and course of infection. (Sundqvist, 1976, Moller, 1981)
 22
Pulpal infection can be through: caries; dentinal tubules direct exposure, trauma, periodontal
disease (lateral canals, accessory canals), operative procedures, leakage around restorations, Cracks
and Anachoresis.

Infectious disease is the result of the interplay between:

• Microbial virulence
• Population density (bacterial load)
• Host defences

(Newton, 2009) several studies have shown that there is little or no correlation between clinical
diagnosis findings and the histopathologic state of the pulp.

Prevalence of periapical disease:

(Eriksen 2006) 1973,1983,1993,2003 cross-sectional 35-year olds Oslo, Norway study

(comparison):
• Prevalence: (16%) had at least one tooth with apical periodontitis; 2003
• Prevalence of root filled teeth and apical periodontitis remained unchanged during the past 10
years.
• A gradual increase in root filled teeth with apical periodontitis from 1973 to 2003 was
observed.

Question 7: Types of endodontic emergencies, treatment and when do you prescribe

antibiotics?
 23
“Endodontic emergencies are usually associated with pain and/or swelling and require immediate
diagnosis and treatment, caused by pathoses in the pulp or periradicular tissue”

Can be classified into:

1. Pre-treatment Emengency: patient is seen initially with severe pain and/or swelling. Often
more difficult to manage than the other two groups. (AAE, 2009)
▪ Pulpal:
o Reversible Pulpitis.
o Symptomatic Irreversible Pulpitis
▪ Periradicular:
o Symptomatic Apical Periodontitis.
o Acute Apical Abscess.
▪ localised swelling
▪ Diffuse swelling (spreading Cellulitis)
2. Inter-appointment emergency (flare-up): after an endodontic appointment but before final
obturation.
3. Post-obturation (post-treatment) emergency: after completion of endodontic treatment
(e.g. obturation). Also called flare-up.

Pulpal emergencies:

Reversible Pulpitis: Clinical condition associated with subjective and objective findings indicating
presence of mild inflammation of the pulp. If the cause is eliminated then the pulp is likely to return to
its normal state. (AAE, 2009)
Management: Emergency treatment: vital pulp therapy
- Indirect pulp capping (stepwise excavation with/without reopening).
- Direct Pulp cap (iatrogenic pulp exposure).
- Partial pulpotomy, Cvek’s technique (carious pulp exposure).
- Complete pulpotomy (cervical pulpotomy).
• Should the symptoms persist and the level of pain increase in duration and intensity, then the
pulpitis is likely to be irreversible.

Irreversible Pulpitis: Clinical condition associated with subjective and objective findings indicating
presence of severe inflammation of the pulp. Often a progression from Reversible Pulpitis. (AAE, 2009)
Management: Emergency treatment options:
• Coronal pulpotomy to relieve pain: acute pain of pulpal origin when there is insufficient time to do a
complete Pulpectomy
• Partial pulpectomy (extirpation with broaches).
• Complete shaping and cleaning of root canals, if time permits (preferred treatment).
• Extraction. If unrestorable, poor prognosis or patient choice.
▪ Plus, Prescribing analgesics (painkillers)
▪ Antibiotics are NOT indicated for Irreversible Pulpitis:
o Adverse reaction (allergy).
o Increase bacterial resistance.
Management of Hyperaemic pulp (Hot pulp):
Supplementary anaesthesia can be obtained with the following:
• Additional infiltration anaesthesia, such as long-buccal, lingual and palatal.
• Inter-ligamentary injection.
• True intra-osseous injection.
• Intra-pulpal anaesthesia.
• Inhalational sedation with local anaesthesia.

Periapical emergency:
 24
Symptomatic Apical Periodontitis: represents inflammation usually of apical peridontium
producing clinical symptoms involving a painful response to biting or percussion or palpation. This may
or maynot be accompanied with radiographic changes (AAE, 2009)
Management: Same emergency treatment options for Irreversible Pulpitis (partial or complete
Pulpectomy), plus reducing the occlusion to eliminate the occlusal contact.

Acute Apical Abscess: is an inflammatory reaction to pulpal infection and necrosis characterized
by rapid onset, spontaneous pain, extreme tenderness of the tooth to pressure, pus formation and
swelling of associated tissues. May not be radiographic signs. Patient often experience malaise,
fever and lymphadenopathy. (AAE, 2009)
Management: Emergency treatment options:
• Localised swelling:
o Pulpectomy. Complete chemomechanical preparation of root canals.
o Drainage: (relief pressure and pain +Removal of a very potent irritant (purulence):
o Through root canals. Not always possible because often the abscess is NOT in communication
with the apical foramen (or blocked canals). However, do not leave tooth open to drain.
o Incision and drainage: The incision should be made at the site of greatest fluctuance and the
clinician should then dissect gently to the bone overlying the root of the tooth causing the
problem.
o Extraction and drainage through the socket (if extraction is the preferred treatment option).
o Often a combination of the first two methods is used
o Occlusal reduction.
o Extraction and drainage through the socket (if unrestorable, poor prognosis or patient choice)
o Plus, Prescribing analgesics (painkillers)
o Antibiotics are NOT indicated for Acute Apical Abscess with localised swelling and
WITHOUT systemic involvement.

• Pulp Necrosis with Diffuse Swelling (Cellulitis): Rapidly progressive and spreading swellings,
not localised and may have dissected into facial spaces. Occasionally associated with systemic
involvement, such as:
• Elevated temperature.
• Lymphadenopathy.
• Malaise.
• Tachycardia (increased heart rate).
• Increased respiratory rate.
Management:
o Pulpectomy. Complete chemo-mechanical preparation of root canals to remove irritant, if
possible; or
o Extraction
o Drainage: often does not occur.
o Plus, Prescribing analgesics (painkillers)
o Systemic antibiotics are indicated for the diffuse, rapidly spreading swelling. Studies
show that odontogenic abscesses reveal a polymicrobial infection, with anaerobic
species predominating:
• First choice, Penicillin (or Amoxicillin) 500 mg tds for 7 days.
• If no improvement in symptoms, Metronidazole can be added to Penicillin. 400 mg tds for 7
days.
• Patients allergic to Penicillin. Clindamycin 300 mg qds for 7 days.
o Hospitalisation: If the infection is spreading into multiple spaces or severe systemic
involvement, this requires hospitalization and aggressive treatment usually by an Oral Surgeon
or a Maxillofacial Surgeon. At the hospital:
• IV antibiotics.
• Incision.
 25
• Placement of several drains.

Ludwig’s Angina: A dangerous bacterial cellulitis in the submandibular and sublingual spaces.
Usually develops from a dental infection in a lower molar. Other causes, tongue piercing.
• Mortality rate 8-10%. Cause of death is usually obstruction of the airway.

Inter-appointment Emergency (Flare-up):

A flare-up is an acute exacerbation of periradicular pathosis after the initiation or continuation of RCT.
(also include after vital pulp therapy and endo surgery NOT only RCT.)
• Properly controlled prospective studies show an overall incidence of 1.8% to 3.2%
• Possiple causes:
• More likely in teeth with PA diagnosis of Symptomatic Apical Periodontitis or Acute
Apical Abscess. Presence of a PA radiolucency is a risk factor.
• Over-instrumentation
• Intra-canal medications, irrigants
• Exposure of the pulp
• Fracture of the root or crown
Management and prevention measures:
• Completion of the chemo-mechanical procedures in a single visit
• Use of an antimicrobial intracanal medicament between appointments in the treatment of
infected root canals.
• Not leaving teeth open for drainage.
• Maintaining the aseptic chain during intracanal procedures.

Post-obturation Emergency:

True post-obturation emergencies are not common. However, mild pain is common for 1 to 3 days
after obturation. Symptoms usually resolve spontaneously. Therefore, reassurance and prescription of
anaelgesics are usually helpful.
• Possible causes:
• High restoration.
• Overfilling (extruded root filling).
• Under-filling (short root filling).
• Root fracture.
• Periodontal therapy.
Management:
• High restoration: Check the occlusion and reduce the high contact.
• Overfilling:
o Prescription of analgesics and, if the pain is more severe and infection is present,
antibiotics.
o An attempt at removal of the root filling and re-preparation of the root canal.
o Periradicular surgery and apicectomy.
• Under-filling (short root filling):
o Usually indicated or associated with inadequate shaping and cleaning (chemo-mechanical
preparation). Infected debris is still present.
o If signs and symptoms persist, then retreat (re-RCT).
• Root fracture:
o Usually poor prognosis, especially if vertical. Extraction is the treatment in most cases.
o Note: if multi-rooted tooth then hemisection or root resection is indicated.
 26

ASA→ Aspirin like drugs (NSAIDS)

APAP→ Acetaminophen (Paracetmol)

Endodontic Emergencies also include Traumatic Dental Injuries.

ESE position statement on antibiotics use, 2018:

Adjunctive systemic antibiotic treatment in conjunction with endodontic therapy is indicated in

the following (Segura-Egea et al. 2017):
• Acute apical abscess in medically compromised patients;
• Acute apical abscess with systemic involvement (localized fluctuant swellings, elevated body
temperature >38°C, malaise, lymphadenopathy, trismus)
• Progressive infections (rapid onset of severe infection in <24 h, cellulitis or a spreading infection,
osteomyelitis) where onward referral to oral surgeons may be necessary;
• Replantation of avulsed permanent teeth (Hinckfuss & Messer 2009, Segura-Egea et al. 2017). In
these cases, topical administration of antibiotics may also be indicated (Andersson et al. 2012).
• Soft tissue trauma requiring treatment (e.g. sutures, debridement) (Diangelis et al. 2012)

Adjunctive systemic antibiotic treatment during endodontic therapy is not indicated in the
following (Agnihotry et al. 2016, Segura-Egea et al. 2017):
• Symptomatic irreversible pulpitis (pain, with no other symptoms and signs of infection);
• Pulp necrosis;
• Symptomatic apical periodontitis (pain, pain to percussion and biting and widening of periodontal
ligament space);
• Chronic apical abscess (teeth with sinus tract and periapical radiolucency);
• Acute apical abscess without systemic involvement (localized fluctuant swellings).
• From current knowledge (Segura-Egea et al. 2017) and based on the International Association of
Dental Traumatology (IADT) guidelines (Andersson et al.2012), antibiotic administration is not
indicated in the treatment of tooth fractures, concussion, subluxation, luxation injuries and extrusion.

Recommended adjunctive antibiotic, (ESE, 2018):

 27

Antibiotic prophylaxis in endodontic therapy, (ESE 2018):

Question 8: how do you achieve endodontic diagnosis (history and examination, sensibility
tests)? And list the indications of use of CBCT in endodontic:
 28

History: is the first step to gather information of origin of pain:

1- Presenting complain and history of complain:
➢ Chronological events that lead to pain: Nature of Problem: Pain, discomfort, etc…
➢ History of dental pain (5 basic directions):
◦ Localization (origin and radiation)
◦ Character and intensity. (Sharp, shooting,dull,aching,,, etc.)?
◦ Duration and frequency. (How often)?
◦ Exacerbating / Relieving (when does it start, What makes it worse, better)?
◦ Associations. (Any associate with)?

2- Medical history and dental history:

➢ Evaluate medical conditions and medications that may alter endodontic treatment.
➢ Preventive measures for infective endocarditis (IE), hx. of bleeding, cardiac or respiratory dx. ,
allergies, artificial joint or organ transplant, bisphosphonates or radiation therapy.
➢ Segura-Egea et al. 2015, reported that there is evidence associating Diabetes mellitus with a
higher prevalence of AP, and delay/arrest of periapical repair.
➢ The prognosis for RFT is worse in diabetics, with a higher rate of RCT failure with increased
prevalence of persistent chronic AP.
➢ Dental Hx.: Restorations, carious tooth fractures, cracks

3- Examination:
➢ ExtraOral examination: (visual and palpation)
◦ Lymph nodes: may be tender especially with acute symptoms.
◦ Facial swelling: usually unilateral, localized or diffuse, firm or fluctuant, Facial spaces
◦ Temperature.
◦ Sinus tract stoma on the skin of the face.
➢ IntraOral examination: (palpation, percussion, mobility, perio. examination) both test and control:
◦ Swellings: exclude non-endodontic causes, Swellings of anterior palate are associated with
lateral incisors, Posterior palate swellings are associated with palatal roots of molars.
◦ Sinus tract and pus: Most sinus tracts are lined with granulation tissue not epithelium.
◦ On palpation compare swellings and bony expansion to contralateral tissues.
◦ Percussion: The aim of this test is to determine the presence/absence of inflammation in the
apical periodontium. However, a negative percussion test does not rule out the presence of such
inflammation.
◦ Palpation: This test is used to detect inflammation in the mucoperiosteum around the root of the
tooth to detect tenderness, fluctuation, hardness or crepitus before extensive swelling is present.
 29
◦ Mobility: : Miller (1950) classification
0 (physiological) 0.1 - 0.2 mm in horizontal direction
I 0.2 – 1mm.
II > 1mm.
III severe mobility vertical and horizontal.

4- Special tests: The main reasons for doing pulpal test are to reproduce the symptoms, to
localize the symptoms and to access the severity of the symptoms. Always use control tooth in
contralateral side for comparison of response (Normal vs. diseased):
➢ Thermal testing: The positive response is an indication that the pulp is vital but does not indicate if
inflammation is reversible, while the negative response is highly indicative of pulp necrosis.
o Heat: using heated GP, or syringe with hot water, usually delayed response (10s)
o Cold: dry ice (frozen CO2) or refrigerant spray.
➢ Electric pulp testing: electric current to stimulate the sensory nerves of the dental pulp, specifically,
the fast conducting myelinated fibers (A-Delta) at the pulp dentin junction. Only indicates that some
sensory fibers are present within the pulp tissue and are capable of responding to the stimulus.
➢ Laser Doppler Flowmetry: It utilizes a light beam, which is scattered by moving red blood cells,
Back scattered light picked by photodetectors, Measures the velocity of moving RBC. i.e. pulpal
blood flow. Disadvantages: expensive, time consuming.
➢ Pulp Oximetry: This gives the percentage of oxygenation of blood, and pulse rate. Use 2
wavelengths to measure ratio of oxygenated/deoxygenated blood. This method has the
potential of not only assessing the presence of a vital pulp but also of assessing pathological
process. (Conflicting evidence)
➢ Bite test: using tooth sloath, may help localise the pain.
➢ Test cavity: small CI test cavity without anaesthesia
➢ Trans illumination: to diagnose cracks, using fiberoptic light probe to the surface may reveal
extent of fracture.
➢ Staining Methylene blue dye: penetrate into cracks
➢ Selective anaesthesia: to localize (mandible vs. maxilla) and when pulp testing are inconclusive

5- Radiographs:
➢ Periapical radiographs being the most common and generally the most useful images.
➢ Sometimes we required other images such as bitewing radiographs, panoramic radiographs,
computed tomography (3D), cone beam scanning, etc. Which can be useful for some cases.
➢ A systematic review done by Kruse et al. 2015, showed the CBCT detect the periapical lesion
with high accuracy, compared to both PR and PAN, but CBCT does not reflect the histological
status of periapical tissue.
➢ Current information does not support a conclusion that the use of CBCT is beneficial for the
patient.

Sigurdsson, Pulpal diagnosis, Endodontic Topics 2003, 5, 12-25.

European Society of Endodontology position statement: The use of CBCT in Endodontics: (Patel,
et al. 2014):

Limitations of conventional radiographic techniques:

• Tow dimensional nature of the images
 30
• Anatomical noise masking the area of interest
• Geometric distortion

❖ A CBCT scan may only be considered after a comprehensive clinical examination has been carried out,
and appropriate conventional radiographs have been taken and assessed.
❖ As with any device emitting ionizing radiation, the benefits of the CBCT scan must outweigh the risks
(ICRP 2007). This is particularly important in children and adolescents who are more radiosensitive to
the potential effects of ionizing radiation
❖ The ALARA principle (“as low as reasonable achievable”) has to be considered in all cases.
❖ A request for a CBCT scan should only be considered if the additional information from reconstructed
three-dimensional images will potentially aid formulating a diagnosis and/or enhance the management of
a tooth with an endodontic problem(s).

Cone Beam Computed Tomography with a limited field of view (FOV) may be considered in the
following situations:
1- Diagnosis of radiographic signs of periapical pathosis when there are contradictory (nonspecific)
signs and/or symptoms;
2- Confirmation of nonodontogenic causes of pathosis;
3- Assessment and/or management of complex dento- alveolar trauma, such as severe luxation
injuries, suspected fracture of the overlying alveolar complex and horizontal root fractures, which
may not be readily evaluated with conventional radiographic views;
4- Appreciation of extremely complex root canal systems prior to endodontic management (for
example, class III & IV dens invaginatus);
5- Assessment of extremely complex root canal anatomy in teeth treatment planned for nonsurgical
endodontic re-treatment;
6- Assessment of endodontic treatment complications (for examples, [post] perforations) for treatment
planning purposes when existing conventional radiographic views have yielded insufficient
information;
7- Assessment and/or management of root resorption, which clinically appears to be potentially
amenable to treatment.
8- Pre-surgical assessment prior to complex periradicular surgery (for example posterior teeth).

Diagnostic Terminology by AAE consensus statement, 2009:

 31

Treatment planning:
 32
➢ Restorative considerations:
Restorative treatment plan should be made before initiating endodontic treatment.
Removal of all restorations, caries and cracks can be called “investigation” of the tooth and it is during
this phase of treatment that the long-term prognosis and the future restorative treatment needs of the
tooth can be assessed. (Abbott, 2004):
◦ Data was collected in regard to 245 restored teeth from 220 patients referred for
endodontic treatment.
◦ Pre-operative examination revealed 47 ( I9.2%) teeth had caries, 57 (23.3%) had
cracks and 96 (39.2%) had marginal breakdown.
◦ After restoration removal, the figures were 211 (86.1%) 147 (60%) and 244
(99.6%) respectively.
◦ Almost all teeth (93%) had more than one of these factors and periapical
radiographs were unreliable indicators of their presence.
Tooth restorability index: by (Mcdonald, 2004):

Revise

The Dental Practicality Index –assessing the restorability of teeth (Dawood & Patel, 2017)

Reeh et al. 1989 concluded that endodontic procedures reduced the relative stiffness by only 5%. An
occlusal cavity preparation, on the other hand, caused a 20% reduction of cuspal stiffness and MOD
cavity preparation caused a 63% reduction. Therefore, endodontic procedures do not weaken teeth
with intact marginal ridges.

Vire DE. 1991, Evaluated the cause of failure for 116 teeth were extracted over a 1-yr period. They
were classified into major failure categories of prosthetic, periodontic, and endodontic origin.
▪ Of the teeth, 59.4% were prosthetic failures which were due primarily to crown fracture.
Teeth that had been crowned had greater longevity than uncrowned teeth.
▪ Periodontal failures constituted 32% of the study.
▪ Only 8.6% of the failures were due to endodontic causes.

➢ Endodontic therapy or implant:

No RCT to compare between implants & endodontic therapy
Comparable outcome for both:
Single implant: success 84.8%, survival 97.2% over 5 years. Jung et al 2012(Clin Oral Implants Res)
NSRCT: success 83%, survival 95% over 4 years. Ng et al 2011(IEJ)

Question 9: Define orofacial pain and mention management of atypical facial pain, burning
mouth syndrome, trigeminal neuralgia?
 33
Orofacial pain: a complaint that around the world affects millions of people on daily basis. It
constitutes any symptoms that occurs from a large number of disorders and diseases that results in a
sensation of discomfort or pain felt in the region of: Face, Mouth, Tongue, Nose, Ears, Sinuses, Eyes,
Neck, TMJ, Head, Throat. Can be:
• Odontogenic orofacial problems:
▪ Dentine hypersensitivity.
▪ Pulpal and Periradicular conditions.
▪ Periodontal abscess.
▪ High restoration.
▪ Cracks & fractures +/- pulpal involvement.
▪ Pericoronitis.
▪ Traumatic Dental Injuries.
▪ rare conditions: cysts or neoplasia (benign/ malignant)
• Non-odontogenic orofacial problems (neuropathic, vascular or TMJ):
▪ Sinusitis.
▪ Post-herpetic neuralgia.
▪ Trigeminal neuralgia.
▪ Glossopharyngeal neuralgia.
▪ Migraine and related variants.
▪ Atypical odontalgia.
▪ Atypical facial pain.
▪ Burning Mouth Syndrome.

Non-odontogenic pain (referred pain) which include:

1. Musculoskeletal origin:
➢ Myofascial pain: Pain of muscular origin appear to be the most common (more than 50 %),
Typically the pain is described as a diffuse, constant, dull, aching sensation.
◦ Lack of symptoms after pulp testing and percussion and/or palpation sensitivity, and/or
failure to resolve symptoms with LA.
◦ Jaw function and palpation of the masticatory muscle(s) will elicit toothaches of myofascial
origin
◦ Typically, local anesthetic infiltration into the trigger point(s) will lead to resolution of
symptoms
◦ Management:
o Deep massage and relaxation techniques
o “Spray and stretch” involves application of a vapor coolant spray to the skin
overlying the trigger point followed by a gentle stretching of the muscle.
o Trigger point injections are used for both the diagnosis and treatment of myofascial
pain
o Muscle relaxants
o Electrotherapy (electrical stimulation (TENS)

➢ TMD

2. Neurovascular pain: headache disorders

◦ Pain can be intense, often pulsatile, and are known to occur only in the head
 34
◦ Most commonly people report pain presenting in the forehead, back of the head, and
temples but also in the sinuses, jaws, and teeth
◦ Primary neurovascular pain disorders are referred pain phenomenon→Intracranial
branches of the trigeminal nerve become sensitized and the associated pain and symptoms
are felt in the somatic structures of the head
◦ These primary headache disorders can be grouped into three major subdivisions:
o Migraine: most likely to present as toothache, unilateral, pulsatile, moderate to severe
intensity, may be with nausea, vomiting, photophobia, phonophobia last from 4-72 h→
relived by NSAIDs or Triptans
o Tension-type headache:
o Cluster headache: Unilateral pains defined by the concurrent presentation of at least
one ipsilateral autonomic symptom, Such as nasal congestion, lacrimation, eyelid
edema, periorbital swelling, or facial erythema, that occurs with the pain. Last between
15 min-2h, that occur in clusters (episodes)

3. Neuropathic pains: Arises from abnormalities in the neural structures themselves (Neuralgia,
Neuroma, Neuritis). The clinical examination generally reveals no somatic tissue damage and
the response to stimulation of the tissue is disproportionate to the stimulus:
◦ Trigeminal neuralgia: (non-odontogenic, neuropathic pain)
o An intense, sharp shooting pain that is most often unilateral, most common mandibular N
o The area that elicits the pain is referred to as a trigger zone (gentle touch to lips, cheeks
or gingiva)
o The response to the stimulus is not proportional to the intensity of the stimulus.
o Slight pressure on a trigger zone results in severe pain.
o Once triggered, pain typically subsides within a few minutes until triggered again.
o Triggers that elicit this type of pain may include chewing and may lead both the patient
and clinician to think of a diagnosis of odontogenic pain.
o Anesthetizing the trigger zone may result in a diminution of symptoms.
o Presents in individuals more than 50 years of age
o The etiology unknown but is thought to be irritation/compression of the root of
trigeminal nerve possibly as a result of carotid artery pressure
o Individuals with multiple sclerosis will develop trigeminal neuralgia more frequently
than the general population For this reason, a person less than 40 years of age who
develops trigeminal neuralgia should also be screened for multiple sclerosis or other
intracranial pathosis.
o 15% to 30% of patients have secondary reasons related to their pain such as brain
tumors and multiple sclerosis.
o Management:
▪ Pharmacological (Carbamazepine, Oxcarbazepine, Baclofen, Gabapentin)
▪ Surgical
◦ Burning mouth syndrome (BMS): as a ‘distinctive neuropathic entity characterized by bilateral
burning oral mucosal pain, usually affecting the anterior two thirds of the tongue, that may
comply with the anatomy of peripheral nerves.
o Within general population 0.7 to 15%
o Increases with age affecting more female than male varying 0.6% in 30 to 39 increasing
to 12.2 by their seventh decade.
o In many patients, neuropathic pain is absent during sleep but occurs at mild to moderate
level in the morning and pain increases throughout the day similar to other neuropathic
pain.
o Aetiology: Originally thought to be purely psychogenic in origin, however, it’s a
complex condition involving the peripheral nervous system, central nervous system,
psychometrics and perhaps genetics.
▪ In 50%, the onset is spontaneous, with no identifiable precipitating factor
▪ 30% cite onset caused by dental procedure, recent illness or medication course
 35
o To diagnose BMS only on exclusion of factors: oral candidiasis, xerostomia,
nutritional deficiency (lower levels of B12, B1, B2, B6 and zinc), H. pylori and GI
disease, diabetes, hypothyroidism, anxiety, poorly fitting prosthesis causing mechanical
trauma, altered taste.
o Management
▪ Cognitive therapy is the only evidence based treatment for BMS
▪ Medical treatment is similar to other neuropathic pain conditions. Medications
include, tricyclic antidepressants, benzodiazepines, anticonvulsants, capsaicin,
topical clonazepam.

◦ Neuroma: A proliferative mass of disorganized neural tissue at the site of a traumatically or

surgically transected nerve (amputation neuroma)

◦ Neuritis: A condition caused by inflammation of a nerve or nerves secondary to injury or

infection of viral (HSV, HZV) or bacterial etiology. Neuritic pain typically is a persistent, non
pulsatile burning and is often associated with sensory aberrations such as paresthesia,
dysesthesia, or anesthesia

4. Psychogenic toothache: (A typical facial pain) mental disorder, somatic pain lacks physical
cause. The pain may be felt in multiple teeth and the pain may jump around from one tooth to
another. Pain that crosses anatomic distribution of peripheral nerves.
o Management: Early identification of psychogenic pain and referral to a psychologist or
psychiatrist is necessary to avoid irreversible and unnecessary dental treatment.

5. Pain associated with a pathologic or inflammatory process:

o Cardiac and thoracic structures: crushing substernal pain that most commonly radiates
to the left arm, shoulder, neck, and face
o Craniofacial structures: tumors in maxillary sinus and jaw, metastatic dx. In mandible
The clinical presentation is highly variable but a common feature is sensory loss along the
distribution of the nerve
o Arteritis: A history of eyesight changes, such as blurred vision, and the examination feature
of pulseless, indurated temporal arteries that are painful to palpation.
o Sinusitis: bacterial or allergies.

Question 10: List types of local anesthesia, constitutes, and mention benefits of
vasoconstrictors?
 36
L.A. a decrease permeability of the ion channels to Na. decreasing the rate of rise of action potential
and its conduction velocity. (Reversible prevents transmission of the nerve impulse in the region to
which it is applied)
• MOA: L.A. uncharged molecule cross the nerve membrane, inside the nerve it form the acidic
charged form which blocks the sodium channels by binding to the inner pore of the sodium
channel. i.e. blocks the rapid sodium inrush to the cell during nerve impulse propagation
Constitutes:
• Local anaesthetic are available as salts (lidocaine hydrochloride) 2% (20mg/ml)
• Vehicle to make solution (dissolved in either water or saline (Ringer’s solution).
• Vasoconstrictor agent (Epinephrine 1:80,000 (0.012 mg)
• Preservative for VC (anti-oxidant): Methylparaben 0.1%
• Reducing agent: Sodium Metabisulphite 0.5 mg
• Fungicide: Thymol
• To adjust pH: sodium hydroxide

Types according to chemical linkage:

• Amino amides (relatively resistant to hydrolysis); lidocaine, mepivacaine, prilocaine, bupivacaine
and
• Amino esters (readily hydrolysed in aqueous solution); cocaine, procaine, tetracaine,
chloroprocaine, benzocaine

Vasoconstrictors: are drugs that constrict blood vessels and thereby control tissue perfusion.
Functions of vasoconstrictor: Epinephrine: act directly on both alpha and beta adrenergic receptors.
➢ Constricting blood vessels and decreasing blood flow to site of administration→ Decrease bleeding
at the site (haemostasis)
➢ Lower the absorption into cardiovascular system→ lower LA in blood→ minimizing risk of toxicity
➢ Increased amount of LA remain in and around the nerve for longer periods→ increasing duration and
depth of anaesthesia)

Question 11: Trauma to central incisor, resulted in discoloration, mention management and
side effects of bleaching (root resorption)?
 37
Trauma to the tooth causes intrinsic type of discoloration due to either:
• Enamel hypoplasia Yellow brown or white
• Pulp haemorrhage products Grey brown or black
• Root resorption. Pink spot

Inadequate awareness of discoloration potential of endodontic procedures and materials may results
in tooth discoloration. Parachloralanine ppt
Intra-endodontic procedures:
✓ inadequate removal of pulp tissues (RBC)→ haemosiderin→ haemolysis→ iron→black ferric
sulphate+ hydrogen sulphide by bacteria→ grey discoloration
✓ Root canal irrigants (NaOCL with CHX→ dark brown parcipitate, NaOCL +MTAD→ brown)
✓ Intra-canal medicaments (Ledermix paste, triple antibiotic paste, formocresol)
✓ Endodontic filling materials (GP,→ pink, AH26 epoxy resin sealer→ green and then black, grey
MTA)
Post-endodontic procedures:
✓ Metallic posts and restorations
✓ Improper selection/application of tooth-coloured restorations
✓ Improper selection/application of crowns and veneers

Management of internal discoloration:

1- Removal of the cause.
• Adequate extension of the access cavity and removal of the cause of the discoloration (e.g.
remaining pulp tissue, medicament, root canal filling material or defective coronal
restorations) is required before internal bleaching. (Abbott 1997).
2- The tooth should then be re-evaluated because the colour may become satisfactory once the cause has
been removed.
3- Non-vital bleaching:
Peroxide chemistry: release free radicles that Breaks down double bonds in chromophore structure of
organic molecules to produce simpler molecules that absorb less light and change the stain to a lighter
colour.

• Walking bleaching: The current technique involves sealing in 10% carbamide peroxide instead
of sodium perborate without needing to mix the product, simply syringing the gel into the cavity and
reviewing the patient in 3 days. (Sulieman 2008):
1- Record initial shade (ideally with photograph of shade tab)
2- Complete RCT and remove GP 2mm below the CEJ to enable a barrier of GIC / ZnOE to be
placed to the level of the CEJ
3- Removal of the smear layer within the access cavity prior to bleaching enhances the penetration
of the bleaching agents into the dentine but this is somewhat controversial (Attin et al. 2003,
Plotino et al. 2008)
4- Place cotton wool soaked with 10% carbamide peroxide in access cavity and temporize
5- Review and replace weekly for 3 weeks
6- If shade improvement satisfactory restore with composite 2 weeks after last bleaching session (to
dissipate residual oxygen within the tooth structure) Why not replace every 2 hours like
7- Photograph of new shade inside/outside bleaching?

• Inside/outside bleaching: This technique is a combination of internal bleaching of non-vital teeth

with the home bleaching technique:
1- Construct suckdown splint with labial and palatal reservoir for tooth or teeth requiring
bleaching only
2- Remove GP 2mm below the CEJ to enable a barrier of GIC (e.g. Chemfil Rock) to be placed
to the level of CEJ (This stage is critical to limit cervical resorption and must be placed
accurately)
 38
3- Give patient suckdown and syringe of bleaching agent (10% carbamide peroxide) with
instructions on placement
4- Patient to apply gel within the access cavity and suckdown splint for designated tooth /
teeth to be bleached only
5- Patient to change gel every 2 hours (working time of the bleaching agent).
6- Review 3-5 days
7- If shade improvement satisfactory clean access cavity to remove plaque biofilm with
sodium hypochlorite and a periodontal ultrasonic followed by water from 3 in 1 to remove
residual irrigant
8- Restore with composite after 2 weeks (to dissipate residual oxygen within the tooth
structure)
9- Photograph of new shade

Generally, the short- and long-term prognosis of internal bleaching is favorable and acceptable to
the patient, as long as the coronal restoration is maintained with no marginal breakdown that could
lead to further discolouration
(Rotstein et al. 1993, Glockner et al. 1999, Abbott & Heah 2009)

Other treatment options:

If bleaching does not provide satisfactory outcomes:
More invasive aesthetic treatment such as the placement of a labial porcelain veneer or a full
coverage ceramic crown may be indicated.

(Ahmed et al, 2012)

Bleaching agents in high concentrations (such as 30% of hydrogen peroxide) combined with heat
(thermocatalytic technique) increase the risk for external invasive root resorption.
(Dahl & Pallesen 2003)

Cervical root resorption : (Invasive cervical resorption):

• Characterized by its cervical location and invasive nature
• Clinically obvious pinkish color in the tooth crown.
A clinical classification has been developed as a guideline for treatment planning and for comparative
clinical research:

Classification of Root Resorption By Lindskog 2006

• Trauma induced tooth resorption;
Surface.
 39
Pressure.
Orthodontic.
Replacement.
Transient apical (Internal).
• Infection induced tooth resorption;
Internal inflammatory.
External inflammatory.
Communicating internal and external.
Hyperplastic invasive tooth resorption;
Internal invasive resorption.
Coronal invasive.
Cervical invasive.

Classification of Root Resorption By Andreasen

• Internal Resorption;
Inflammatory Resorption.
Replacement Resorption.
Transient Apical Resorption.
• External Resorption;
Surface Resorption.
Inflammatory Resorption.
Replacement Resorption.
 40
Question 12: Mention different procedures for vital pulp therapy and their outcome:

Vital pulp therapy: “Procedures that are designed to maintain the health of all, or part of the
pulp”(ESE, Quality guidelines of endodontic treatment, 2006).
Aims:
✓ Relieving painful symptoms of pulpitis
✓ Preventing the development of a destructive course of pulpal inflammation and subsequent
infection of the root canal space.
✓ Formation of reparative dentin.
✓ Continued root development in immature permanent teeth (open apex).

Procedures:

Indirect pulp capping: described by John Tomes in 1859. Defined as a procedure in which a pulp is
covered with a protective dressing or cement placed over a thin partition of remaining dentine or
slightly softened dentine which if removed, might expose the pulp:
➢ Stepwise excavation: : is procedures whereby caries is excavated in a stepwise fashion in
order to prevent iatrogenic pulpal exposure. Indications:
• A restorable deep carious lesions, where the bulk of necrotized dentine has not yet reached
the pulp.
• No clinical and/or radiographic signs of pathology such as persistent pain, widened
periodontal membrane or periapical periodontitis.
• Uncomplicated crown fracture.
Technique: (2 stage procedure).
• Rubber- dam; isolation to reduce bacterial contamination.
• First visit; remove infected softened carious dentine .
• Remaining layer of demineralized dentine is covered with calcium hydroxide
• Temporary restoration placed for >2 months to encourage tertiary dentine formation.
• Temporary restoration removed and remaining demineralised tissue excavated Cavity sealer inserted –
varnish/liner/base Permanent restoration placed.

➢ Without re-entry and further excavation: Is similar to stepwise excavation but differs in the
sense that the innermost layer of carious dentine is deliberately and permanently left behind.
 41

Advantages of Indirect pulp capping: :

✓ less aggressive techniques for maintaining the vitality of pulp and giving the pulp a chance to
heal.
✓ Does not expose pulp to micro-organisms in carious dentine or saliva.
✓ Cost effective.
✓ More comfortable and acceptable treatment as compared to various complex endodontic
treatment.

Disadvantages: Issues of concern of indirect pulp capping:

▪ Operative procedures during treatment may create irreversible pulpitis.
▪ Potential for carious process to continue.
▪ Presence of micro-exposures.
▪ Solubility of some (calcium hydroxide) liners over time
▪ Lack of seal provided by some liners (calcium hydroxide).
▪ Limited clinical evidence on outcomes using ‘total etch technique’
▪ Long-term sealability of coronal restoration.
▪ Principle of leaving micro-organisms and diseases tissue (carious dentine) within body
▪ Inability to correctly diagnosis pulp condition on every occasion
▪ Indirect pulp capping without stepwise excavation is not predictable with deep carious lesions-
although some studies describe a high success rate

Direct pulp capping: It’s a process of placing an agent in contact with or in close proximity to the
pulp to encourage formation of new dentine and promote healing of the pulp complex. For a restorable
tooth with reversible (noninfected) pulpitis diagnosed from the history, examination, pulp testing and
radiographs but with an exposed bleeding pulp. Exposure of the pulp can occur as a result of:
▪ Traumatic exposure during cavity preparation
▪ Carious exposure during cavity preparation - direct pulp capping (controversial)
▪ Trauma – direct pulp capping not advised.
Technique:
▪ Apply rubber dam and maintain a saliva free operating site
▪ Carefully remove caries to minimize trauma
▪ Clean pulp wound and tooth tissue with sterile saline
▪ Wash site with sodium hypochlorite to establish haemostasis, destroy micro-organisms and remove
dentine debris
▪ Place MTA on exposed pulp tissue and cover with moist cotton wool and base material
▪ Review, remove cotton wool and check MTA has hardened
▪ Restore tooth with high quality restoration
▪ Long term follow-up to monitor pulp condition and root development.
Concerns:
▪ Size of exposure – large exposures are likely to be infected and the pulp damaged by the operative
procedure
▪ Location of exposure – exposures on the axial wall may cause necrosis coronally
▪ Presence of micro-organisms and further microleakage are more important than choice of capping
agent
▪ Control of HAEMORRHAGE and EXUDATE is essential.
▪ Quality of the dentinal bridge – they are often porous (tunnels)
▪ Inflamed pulps have a poorer outcome than non-inflamed pulps – thus, this technique is controversial
following carious exposure – partial pulpotomy may be preferred.
▪ Long-term sealability of coronal restoration.
▪ Not predictable following carious exposure.
 42
Superficial pulpotomy: removal of the exposed (infected) pulp and dentine surrounding an exposure to
a depth of approximately 2 mm followed by the placement of a wound dressing on the non-infected tissue
▪ Case selection: A restorable tooth with partial pulpitis diagnosed from the history, examination, pulp
testing and radiographs but with healthy, noninfected pulp tissue below the diseased, infected tissue.
Technique:
▪ Apply rubber dam and maintain a saliva free operating site
▪ In carious teeth carefully remove diseased tissue to minimise further trauma to pulp
▪ Amputate pulp with diamond bur with water cooling
▪ Clean pulp wound and tooth tissue with sterile saline
▪ Wash site with NaOCl to establish haemostasis, remove dentine debris and kill micro-organisms
▪ Place MTA on exposed pulp tissue and cover with moist cotton wool and base material
▪ Review, check hardening of MTA Restore tooth
▪ Long term follow-up to monitor pulp condition (and root development)

Key issues: trauma:

▪ Young immature pulps are resistant to microbial invasion following traumatic injuries and inflammation
can remain superficial
▪ Duration of contamination following traumatic exposure is important yet controversial

Concerns:
▪ Microleakage of micro-organisms may be more important than choice of wound dressing agent
▪ Superimposed mechanical trauma during the operative procedure can have a negative impact on the
outcome
▪ Presence of dentine particles may induce increased inflammation
▪ Removal of pulp tissue must be atraumatic
▪ Control of HAEMORRHAGE and EXUDATE is essential - development of a blood clot has a
negative impact on the outcome as it can induce dystrophic calcification and internal resorption, it
also forms a culture medium for bacteria.

Coronal (Cervical) pulpotomy: removal of the diseased (infected) coronal pulp to the level of the
orifice(s) of the root canal(s) and the placement of a wound dressing on the non-infected remaining tissue

The ideal material for vital pulp treatment should be able to resist long-term bacterial leakage and
stimulate the remaining pulp tissue to return to a healthy state, promoting the formation of dentine.
Materials used:
- Calcium hydroxide Cement (CaoH): (Mohammadi & Dummer, 2011):
◦ Caustic effect on superficial pulp tissue up to 0.7 mm – to produce a necrotic layer
◦ A layer of liquefaction necrosis forms under the wound dressing
◦ A layer of coagulated necrotic tissue forms beneath
◦ The coagulated necrotic tissue becomes diffusely calcified
◦ Hard tissue formation occurs beneath as an amorphous tissue that develops into dentine.
◦ Alkaline pH and antimicrobial
◦ Initiates dentine bridge formation in 50- 90% of cases – bridges often have tunnel defects
◦ Soluble, Does not seal well nor prevent microleakage
- Zinc Oxide Eugenol Cement (ZOE)
- Glass Ionomer Cement (GIC)
- Adhesive resin system
- MTA
 43
Outcome:
(Ricketts et al. 2013): Cochrane Systematic Reviews compare three different techniques for
caries removal:
1- Stepwise excavation technique
2- Partial caries removal (without re-entry)
3- No dentinal caries removal
Result:
➢ Stepwise caries removal resulted in a 56% reduction in incidence of pulp exposure
compared to complete caries removal.
➢ Partial caries removal reduced incidence of pulp exposure by 77% compared to complete
caries removal.
➢ No dentinal caries removal had a similar result compared to complete caries removal.
Conclusion:
Stepwise and partial excavation reduced the incidence of pulp exposure in symptomless, vital, carious
primary as well as permanent teeth. Therefore these techniques show clinical advantage over
complete caries removal in the management of dentinal caries.

Guideline on Pulp Therapy for Primary and Immature Permanent Teeth. American Academy of
Pediatric Dentistry (2015, 2016): Current literature indicates that there is no conclusive evidence
that it is necessary to reenter the tooth to remove the residual caries. As long as the tooth remains
sealed from bacterial contamination, the prognosis is good for caries to arrest and reparative dentin
to form to protect the pulp.

Partial pulpotomy Outcome:

▪ 95% of anterior teeth with crown fractures and exposed pulps demonstrated hard tissue barriers and pulp survival (Cvek
M.1978).
▪ 91-93% of symptom-free posterior teeth with carious exposures demonstrated hard tissue barriers and pulp survival
(Mass, Zilberman, 1993)

Cervical pulpotomy Outcome

▪ Following traumatic injuries 72-79% of incisors healed after cervical pulpotomy with calcium
hydroxide (Hallet, Porteus, 1963)
▪ 26 permanent molars with carious pulp exposures and apical periodontitis confirmed
radiographically were treated with pulpotomy using calcium hydroxide. After follow-up for at least
16 months 24 teeth demonstrated dentine bridge formation and normal periapical architecture
(Caliskan, 1995)

Question 13: Mention root canal treatment basis, objectives, steps. Basis of WL determination,
cleaning and shaping and canal obturation. Mention a couple of procedural errors and how to
avoid them?
 44
Endodontic therapy: aims to preserve functional teeth without prejudice to the health of the
patient
When the pulp is diseased or injured, treatment is aimed at preserving normal periradicular tissues or
restoring them to health.
(European Society of Endodontology, 2006)

Canal preparation:
Shaping:- Controlled removal of dentine to produce a suitable shape to facilitate irrigation, the
placement of a medicament, and the insertion of a dense root filling without compromising the
integrity of the tooth. Mechanical objectives: (Schilder, 1974)
o To develop continually tapering funnel form from access to apical foramen (to facilitate
irrigation, medicaments and placement of root filling)
o Maintain the path of original canal (prevent transportation toward outer aspect of the curve in the
apical part, and towards inner side of maximum curvature, avoiding creation of ledges,
perforations and danger zones)
o Retain apical foramen in original position (prevent formation of zips and foramen translocation)
o Keep the apical opening as small as possible (prevent weakening of root, ensure tapered
preparation, maintain better control over instrument, irrigants, medicaments, filling)
o Apical stop: ensure canal is narrowest at apex, flow and integrity
o Patency: involves the periodic passage of small files through the apical foramen in an attempt to
remove dentine debris, pulp tissue and micro-organisms

Instrumentation techniques:
• Hand instruments
• Rotary devices
• Reciprocal devices
• Vibratory devices
• Sonic
• Ultrasonic

Apical Limit (determination of working length):

• Working length can be defined as the distance from a coronal reference point to the point at
which canal preparation and obturation terminate.
• The objective of determining the working length is to enable the root canal to be prepared as
close to the apical constriction as possible. (ESE, 2006)

A histologic study of over than 400 teeth, it described precisely the location of the apical constriction
and its relationship to the apical foramen.
• The foramen of the main root canal may be located to one side of the anatomical apex,
sometimes at distance of up 3 mm in 50 - 98 % of roots.
(Kuttler 1955, Green 1956, Pineda & Kuttler 1972).

The foramen to apical constriction is approximately 0.5 mm in the younger group and 0.8 mm in the
older group for all teeth type.
(Kuttler 1955, Dummer et al. 1984, Stein and Corcoran 1990).

The CDJ position is inconsistent and not ideal landmark to terminate RCT.
Apical constriction is not constant (Dummer et al. 1984)
The anatomical variation in apical constriction location, size, tooth type and age make working length
assessment unreliable.
Following the histological examination of biopsy material from 41 teeth it was concluded that the
most favorable outcome occurred when instrumentation and filling were at or short of the apical
constriction. CDJ is located at different levels on opposite sides of the root canal wall, and does not
 45
coincide with the apical constriction.
(Ricucci, 1988)

Based on biological principles and experimental evidence, instrumentation or filling should not
extend beyond the apical foramen: (Wu et al. 2000)
• Vital pulps 0–2mm short of apex
• Infected pulps –at the canal terminus
• Retreatment –at the canal terminus

Apical limit determination: (tactile, radiograph, apex locator, CBCT, paper point, pt. response):

Disadvantage of radiographs: Inability to visualize canal terminus

40%canal terminus at apex
40% canal terminus –mesial / distal
20% canal terminus –buccal / lingual

Under simulated clinical conditions working lengths of 169 roots were determined radiographically to
within 0-2 mm of the apex. Instrumentation occurred beyond the apical foramen in 51% of premolars
and 22% of molars (ElAyouti et al. 2001)
→Using working lengths determined radiographically in posterior teeth would result in
instrumentation beyond the constriction in a high proportion of cases (66%)
Working lengths determined only using the Root ZX apex locator in premolar teeth resulted in
instrumentation beyond the constriction in 21% of cases (from 51% with radiographs alone).
Combined use of radiographs and apex locator led to overestimation of length in 14% of cases
(ElAyouti et al. 2002)

Principle of Apex locator: (Necoofar et al. 2006) Accurate in reading (90-98% accuracy).

• ElAyouti et al. 2009, they measured the consistency of apex locators.

• They reported the apex locators was consistent in 85% of the patients.(Using Raypex5 & Root
ZX).
• The inconsistency was strongly associated with partially or totally obliterated root canals.

According to ESE quality guidelines for endodontic treatment (2006), recommended

methods are electronic and radiographic.

Cleaning:- Removal of all inorganic debris, organic substrate and micro-organisms

• Sodium hypochlorite solution can: Dissolve and digest endodontic micro-organisms, necrotic tissue
and the organic components of the smear layer, inactivate endotoxin.
 46
• 0.5% sodium hypochlorite solution is more effective than saline solution as a root canal irrigant.
(Byström & Sundqvist,1983)
• The currently available evidence is strongly in favor of sodium hypochlorite solution as the main
endodontic irrigant
• There is no rationale for using sodium hypochlorite solutions above 1%wt/vol
• Cleaning is more effective: in large canals more taper, endosonics, with NaOCl and EDTA/ citric
Acid, and in the coronal and middle thirds
(Zehnder, 2006)
• Concentrated solutions of sodium hypochlorite significantly reduce the elastic modulus and flexural
strength of dentine. (Sim et al. 2001)

Regimen (Zehnder, 2006)

• Following initial opening of pulp chamber – sodium hypochlorite
• During shaping – sodium hypochlorite
• After shaping - saline
• During final debridement – aqueous EDTA (17%) followed by saline and then sodium hypochlorite
• Final rinse to remove chemicals - saline

Canal medication
• Calcium hydroxide is more effective as an inter-appointment medicament than camphorated
paramonochlorophenol and camphorated phenol. (Byström A et al. 1985)
• Calcium hydroxide as an inter-appointment medicament for 7 days efficiently eliminates bacteria
that may survive biomechanical instrumentation. (Sjögren, 1991)
• Application of calcium hydroxide for 4 weeks did not prevent regrowth of residual micro-organisms
(Peters et al. 2002)
• Systematic review and meta-analysis: Calcium hydroxide has limited effectiveness in eliminating
bacteria from human root canals when assessed by culture techniques. (Sathorn, 2007)

Canal filling (obturation+ coronal filling): To control intraradicular re-infection by producing an

inhospitable environment within the root canal system for the survival or growth of residual or new
intraradicular microorganisms.
Functions of filling:
o To entomb surviving micro-organisms and prevent their proliferation
o To prevent movement through the canal system of new micro-organisms entering from coronal
and radicular routes
Coronal restoration and leakage:
In 1987, Swanson & Madison in vitro study showed that after only three days exposure to artificial
saliva there was extensive coronal leakage of a tracer dye through apparently sound root filings.
• Periapical status of endodontically treated teeth in relation to the technical quality of the root filling and
the coronal restoration. (Ray & Trope, 1995)
Percentage of absence of periapical pathosis
Good filling/good restoration 91.4% Poor filling/good restoration 67.6%
Good filling/poor restoration 44.1% Poor filling/poor restoration 18%
• Influence of coronal restorations on the periapical health of endodontically treated teeth. (Tronstad L et
al. 2000)
Outcome (success) of root fillings
Good filling/good restoration 81% Poor filling/good restoration 56%
Good filling/poor restoration 71% Poor filling/poor restoration 57%
Factors that contribute to persistent apical radiolucency: (Nair, 2006)
• There are six biological factors that contribute to the persistence of periapical radiolucency after
root canal treatment:

1. Intra-radicular infection persisting in the complex apical root canal system

 47
2. Extra-radicular infection, generally in the form of periapical: actinomycosis;
3. Extruded root canal filling or other exogenous materials that cause a foreign body reaction;
4. Accumulation of endogenous cholesterol crystals that irritate periapical tissues;
5. True cystic lesions
6. Scar tissue healing of the periapical tissues.

Endodontic Procedural errors and management:

1. Missed canals: major cause of RCT failure. Prevention:

• Radiographic examination
• Adequate access opening
• Use of the operating microscope: (Yoshioka et al. 2005) could detect the MB2 canal in 7% of
cases with the naked eye, in 18% of cases using magnification, and in 42% of cases using US tips
under the operating microscope
• Use of ultrasonics

2. Ledge formation: is an artificial irregularity created on the surface of the root canal wall that impedes
the placement of an instrument to the apex of an otherwise patent canal. Factors involved in ledge
formation:
• Tooth location
• Canal curvature
• Instrument design and alloy properties
• Instrumentation techniques
• Operator experience
Management of ledge: by-pass and blended into canal instrumentation, it has no effect on the
prognosis if it was managed properly.

3. Canal blockage: by dentine chips and/or tissue debris is an obstruction in a previously patent canal that
prevents access and complete disinfection of the most apical part of the root canal system. Could be due
to:
• Instrumentation is not accompanied by copious irrigation
• Instruments are not cleaned before their reinsertion into the canal
Management: re-negotiate the canal to clear blockage. When the blockage cannot be negotiated,
the hardened debris may jeopardize the outcome, particularly in infected cases, as
microorganisms can remain embedded in debris. Prevention through:
• Copious frequent irrigation
• Wiping of instruments before their reinsertion into the canal, and recapitulation during the
entire instrumentation procedure
• The passive use of a flexible, small patency file 1mm longer than the canal terminus

4. Canal transportation: It is the removal of canal wall structure on the outside curve in the apical half of
the canal due to the tendency of files to restore themselves to their original linear shape during canal
preparation; this may lead to ledge formation and possible perforation. Consequences:
• Insufficient cleaning: a part of the original root canal will remain unprepared and thereby
insufficiently cleaned.
• Over reduction of radicular dentine: In curved canals, the outside (convex) wall of the apical portion
may be over instrumented and healthy dentine may be unnecessarily removed. The inside (concave)
wall may be untouched and infected dentine may remain.
5. Perforations: They are mechanical or pathological communications between the root canal system and
the external tooth surface. The incidence of perforations is quoted in the literature as being between 3
and 10%. They can be classified:
• Pre-operative occurrences, typically pathologically, e.g. resorption or decay. (Ng et al. 2011): The
presence of a preoperative root perforation significantly reduced the odds of success by 56%
 48
• Operative procedural accidents, e.g. during access or canal instrumentation
• Post-operative procedural errors, e.g. during preparation of a post-space: (Kvinnsland et al, 1989):
53% of iatrogenic perforations occur during insertion of posts (prosthodontic treatment); the
remaining 47% are induced during routine endodontic treatment.

(Clauder, 2009)
Management:
• Non-surgical: crown, pulpal floor, and furcation: root canals should be instrumented to allow proper
intra-canal medication and closure of the orifices. Generally, in supracrestal perforations, preference
should be given to adhesive materials and in subcrestal regions, to MTA.
• Non-surgical: middle on third of root canal: Before closing the defect, the original canal should be
instrumented to at least a size that allows accurate protection of the canal, thus preventing blockage.
After initial 3-dimensional obturation of the canal apical to the perforation, the defect and the rest of
the canal can be obturated with MTA. The other option is to use a ‘space-maintainer= GP cone or
file’ after hemostasis has been achieved.
• Non-surgical: Apical third: it can be helpful to place a pre-bent file into the original canal, which
stays as a space maintainer. After MTA is placed in the perforation site, the file must be loosened
before MTA sets in order to be able to negotiate the original canal in the next visit
• Surgical intervention is reserved for cases not amenable to, or which have not responded to, non-
surgical treatment. Surgical repair of root perforations has been performed by reflecting a flap at the perforation site
and packing a repair material into the cleaned and usually mechanically prepared defect.

• Overfilling or underfilling: The underfilled root canal fails to seal the circumference of the apical
foramen in one or more dimensions, leaving reservoirs for stagnation of fluids, recontamination and
persistence of infection.
Overfilling material inflammatory response and toxic effect:
• Sealer: All obturation sealers are irritants in their freshly mixed states. After setting or curing, some sealers
lose their irritant components and become relatively inert. Components of sealers will be managed by the
immune system in the process of absorption.
• Gutta-percha: Because of the tissue tolerance of gutta-percha, extrusion of the material in and of itself
should not impair tissue healing.
• Resilon: In a study using human gingival fibroblasts, Resilon alone was no more cytotoxic than gutta percha

As long as the overextension is not in contact with fragile structures, such as the inferior alveolar nerve
or sinuses, and the apical terminus is well filled in three dimensions, permanent harm is potentially small,
unless the obturation materials contain paraformaldehyde.
A period of post-operative observation following root canal therapy ranging from 6 months to 4 years
has been advocated by various investigators.

6. Maxillary sinus perforations: Can happen due to close proximity of maxillary premolars and molars to
the sinus. In general exposure of the sinus lumen is well tolerated but introduction of foreign materials
during the access or apical resection/manipulation can initiate thickening of the sinus mucosa with
symptoms of maxillary sinusitis.
Management: Surgical intervention is the most predictable method for removing extruded root
canal filling material and allowing adequate healing secondary to sinus complications

7. Inferior alveolar nerve injury: extrusion of endodontic materials, over instrumentation, elevated
temperatures) is one of the common causes of IAN injury It has been suggested that it occurs in up to
1% of mandibular premolars that receive root canal treatment. Management:
 49
• If overfilling causes anesthesia and painful dysesthesia, referral to a surgeon (oral-maxillofacial or
neurosurgeon) may be required.
• The oral surgery literature describes most inferior alveolar nerve injuries as ” neuropraxias” and thus
they resolve spontaneously within a 6-month time frame.
• It is suggested that the decision to intervene surgically should include the high suspicion of injury
resulting in the loss of conduction within the nerve because of suspected chemical toxicity and
mechanical compression.

8. Cervecofacial subcutaneous emphysema: It is the penetration of air or other gases beneath the skin
and submucosa resulting in soft tissue distention.
• Compressed air can be delivered through an air syringe or a high speed hand piece and air is
deposited beyond the canal space.
• The majority of cases present as a soft skin coloured swelling without redness that occurs during or
shortly after the dental appointment.
Management:
• Antibiotics prescribed due to the non sterility of the air supply and the possibility of necrotic
debris or micro organisms forced into the surrounding tissue.
• Severe cases may need hospitalization with I.V antibiotics and close monitoring of the
condition.
• It takes 4-7 days for patients to return to their normal appearance.

(NG. et al. 2011: Factors affecting outcome of NSRCT: tooth survival)

Question 14: Mention outcome of RCT and success and survival rates of RCT as well as factors
influencing the outcome?

Clinical criteria of health:

• No evidence of discomfort • No tenderness to percussion
 50
• Normal mobility • No signs of infection or swelling
• No sinus tract • Tooth in function
Radiographic criteria of health:
• Normal/slightly thickened periodontal ligament space
• Elimination of rarefaction
• No evidence of resorption
Histologic criteria of health:
• Healthy tissues with normal periapical architecture and no evidence of inflammation
Pragmatic criteria:
• Tooth in adequate clinical function

Outcome studies:
Factors affecting the long-term results of endodontic treatment. (Sjögren et al. (1990)
Outcome (success) of root fillings
Proportion with normal radiological features
o Vital pulps 96%
o Pulp necrosis (no apical pathology) 100%
o Pulp necrosis (apical pathology) 86%
o Retreatment (no apical pathology) 98%
o Retreatment (apical pathology) 62%

Outcome of primary root canal treatment: systematic review of the literature – Part 1. Effects of study
characteristics on probability of success. (Ng et al. 2007)
Following a comprehensive systematic review of the literature on the outcome of primary root canal
treatment it was concluded that:
o The estimated pooled success rate of treatment was 68% when strict criteria were used
o The estimated pooled success rate of treatment was 85% when loose criteria were used
o The reported success rates had not improved over the last four (or five) decades
o The quality of evidence for treatment factors affecting primary root canal treatment is sub-optimal

Outcome of primary root canal treatment: systematic review of the literature – Part 2. Influence of
clinical factors. (Ng et al. 2008)
Following a meta-analysis to quantify the influence of clinical factors on the efficacy of primary
root canal treatment it was concluded that:
Four conditions were found to improve the outcome:
1- Pre-operative absence of periapical radiolucency;
2- Root filling with no voids;
3- Root filling extending to 2 mm within the apex;
4- Satisfactory coronal restoration.
Concluded that root canal treatment should aim at:
o Achieving and maintaining access to apical anatomy during chemico-mechanical debridement;
o Obturating the canal with densely compacted material to the apical terminus without extrusion
into the periapical tissues;
o Preventing re-infection with a good quality coronal restoration.

Outome of secondary root canal treatment: a systematic review of the literature.

(Ng et al.2008)
Following a meta-analysis to investigate the influence of clinical factors on the efficacy of
secondary root canal treatment it was concluded that:
o The pooled estimated success rate of secondary root canal treatment was 77%;
 51
o The presence of pre-operative periapical lesion, apical extent of root filling and quality of
coronal restoration proved significant prognostic factors.

Tooth survival following non-surgical root canal treatment: a systematic review of the literature.
(Ng et al. 2010).
Following a meta-analysis to investigate tooth survival following root canal treatment it was
concluded that:
The 2-10 yrs. pooled estimated survival rate of root canal treatment was 86% -93%
Four conditions significantly improved tooth survival:
1- Crown restoration
2- Having both M/D contacts
3- Not serving as an abutment
4- Non-molar

A prospective study of the factors affecting outcomes of nonsurgical root canal treatment: part 1:
periapical health. (Ng et al. 2011)
Following a prospective study to investigate periapical health following root canal treatment it
was concluded that:
Complete periapical healing after primary RCT was 83% and after secondary RCT was 80%;
Eleven prognostic factors affected the outcome. The conditions found to improve periapical
healing included:

1- Absence of a periapical lesion 6- Use of EDTA in secondary RCT

2- When lesion present – the smaller its size 7- Not using chlorhexidine
3- Absence of a sinus tract 8- Absence of inter-appointment flare-up
4- Achievement of patency 9- Absence of root filling extrusion
5- Cleaning to the canal terminus 10- Satisfactory coronal restoration

A prospective study of the factors affecting outcomes of nonsurgical root canal treatment: part 2: tooth
survival. (Ng et al. 2011)
Following a prospective study to investigate tooth survival following root canal treatment it was
concluded that:
The four-year tooth survival following primary or secondary RCT was 95%;
Thirteen prognostic factors affected the outcome.
Following a prospective study to investigate tooth survival following root canal treatment the
conditions found to increase tooth extraction included:

1- Diabetic patient or on systemic steroid 6- Periodontal probing > 5 mm;

therapy; 7- Presence of cast post and core;
2- Preoperative pain; 8- Temporary restoration;
3- Preoperative sinus tract; 9- No crown;
4- Inability to achieve patency at canal 10- Terminal tooth.
terminus (within 22 months);
5- Extrusion of filling material (beyond 22
months).

Question 15: Define periodontal disease and list the risk factors for developing the disease?

Periodontal risk factor: “an aspect of personal behaviour or life style, an environmental exposure, or
an inborn or inherited characteristic that changes the susceptibility to periodontal disease”
(Clerehugh 2009)
 52

▪ Microbial plaque is the primary aetiological factor

▪ Risk factors are secondary aetiological and can enhance the development, progression and relapse
or recurrence of disease
▪ Modifiable risk factors: smoking, plaque levels …etc
▪ Non- modifiable risk factors: age, gender or inherited (genetic) conditions

Can be classified to
 Local factors (intra-oral): As microbial plaque is the primary aetiological factor in
periodontal disease, local factors are mainly things that accumulate or attract more plaque in
the oral cavity or plaque retention factors
o Anamotical factors (tooth alignment, crowding, rotations, prominent frenal attachment,
developmental crown and root morphology (enamel pearls -%34 lower molars, %25 upper
molars-, grooves)
o Patient’s habits:
• Mouth breathing (incompetent lips→ decreased Saliva→ dehydration of tissues
o Iatrogenic factors:
• Ortho appliances
• Poor design RPD (gum stripping, not enough gingival clearance)
• Poor crown and restoration margins
• Roughness as a result of instrumentation
o Microbiological factors (some microbes increase breakdown A. actinomycetemcomitans, P.
Gingivalis, B. forsythus)
o Pre-existing deposits and disease (Carious lesions at gingival margins or below Periodontal
disease, Existing pockets more difficult to clean, furcation involvements, Calculus (sub and
supra)
▪ Pocket depth
▪ Severity of attachment loss
▪ Type of bone loss
▪ Furcation involvement
▪ Root morphology- root length- divergence- root trunk length
▪ Anatomical anomalies- grooves- Pits
▪ Quality and quantity of restorations
▪ Bleeding

 Genral factors:
o Environmental: Drugs causing Gingival Hyperplasia: phenytoin (antiepileptic), ciclosporin
(immunosuppressant) and Calcium Channel Blockers (nifedipine, verapamil, amlodipine,
diltiazem), Oral contraceptives associated gingivitis
o Metabolic:
• Hormonal factors: Pregnancy associated gingivitis. Pregnancy epulis. Menstrual cycle
• Diabetes: related to level of glucose control (poorly or well controlled)
o Genetic/ inherited:
o Down syndrome
▪ Aggressive periodontitis,
▪ Defect of neutrophil chemotaxis
▪ Mouthbreathing, poor OH
o Papillon-Lefevre syndrome (Defect of neutrophil chemotaxis and phagocytosis)
o Hypophosphatasia
▪ Low levels of enzyme alkaline phosphatase
▪ Teeth exfoliate
▪ Defective mineralisation
o Ehlers-Danlos syndrome
▪ Disorder in collagen formation
▪ Especially type XIII which leads to severe periodontal destruction
III
 53
▪ Hyperextensible skin

o Behavioural Smoking:
o Clinically, more attachment loss, PD, bone loss, recession, staining and less
bleeding.
o Histologically inhibits neutrophils, more keratinised tissue and less vascular
response to inflammation
o Therapy is less effective in smokers
o Pack years? One pack year = 20 cigarettes per day for one year.
o Lifestyle:
o Stress
▪ Depresses immune system
▪ May lead to worse oral hygiene, increased smoking, less non-emergency dental
visits
o Malnutrition
▪ Vit C deficiency (Scurvy): haemorrhagic Gingivitis
▪ Protein deficiency can lead to loss or destruction of periodontal supporting tissues
o Haematological:
o Chediak-Higashi syndrome: (Can be like localised aggressive periodontitis)
o Neutropenia
▪ Cyclic neutropenia
▪ Gingival ulcerations, gingivitis and periodontal destruction
▪ Familial benign neutropenia
o Leukaemia: (Gingival swelling, and ulceration and excessive bleeding in acute cases)
o Other systemic factors:
Obesity
Dietary calcium (if low)
Male gender (Still unknown, could be because of oestrogen protective effects on bone in females.)
Low socio-economic status
Age (Prevalence and severity)
Non-modifiable:
Age/ age at diagnosis
Genetic factors (family history)
Hormonal factors
Modifiable:
Oral Hygiene
Smoking
Poorly controlled diabetes (?other systemic disease)
Extent/severity/type of bone loss
% pockets>5mm
Bleeding on probing
(Number of missing teeth)

Risk assessment: Qualitative or Quantitative assessments are made of the likelihood for adverse
events to occur Goes beyond identifying the disease but considers factors likely to:
- influence future progression
or
-predict the likelihood of the disease developing
 54
The on-going risk assessment of these patients allow dental practitioners to determine how often
to review them and how much supportive care should they be given: (Lang & Tonnetti, 2003)
 To identify those susceptible to periodontal disease and target preventive measures to
reduce the risk of attachment loss
 Target management to reduce further attachment loss occurring

Uses different risk factors and indicators (parameters) to assess the overall risk of a patient
1. Percentage of bleeding of probing. (Low <9%, moderate <25%, high >25%)
2. Prevalence of residual pockets greater than 4 mm (5 mm)(Low <4. M 4-8, H >8)
3. Loss of teeth from a total of 28 teeth (L <4, M 4-8, H >8)
4. Loss of periodontal support in relation to the patient’s age (L 0.5, M 0.5-1, H >1)
5. Systemic and genetic conditions
6. Environmental factors such as cigarette smoking
Each parameter has low, moderate and high-risk profiles

 Low PRA: all parameters within the low-risk categories or no more than one parameter within
the moderate-risk category
 Moderate PRA: at least two parameters in the moderate category, but at most one parameter
in the high-risk category
 High PRA: at least two parameters within the high-risk category

Sites most at risk of further attachment loss:

▪ Pockets> 6mm
▪ Multi rooted teeth
▪ Furcation involvement
▪ Vertical defects
▪ Poor patient compliance
▪ Systemic factors
▪ Bleeding on probing

Multi level risk assessment

▪ Patient
▪ Mouth
▪ Tooth
▪ Site

Question 16: explain what’s the BPE and comment on its use and limitations and comment on
the parameter of assessing disease activity?

BPE: First developed by the British Society of periodontology in 1986. Relatively quick and simple to
use screening tool that is used to indicate the level of examination needed. (British Society of
Periodontology 2016).
 55
• Provides basic guidance on treatment need.
• The BPE does not provide a diagnosis
• Not for monitoring response for periodontal therapy

The use of a WHO (world health organization) probe:

• A ball-end of 0.5mm diameter
• A colored band extending from 3.5 to 5.5 mm (epidemiological-type probe)
• A second band from 8.5 to 11.5mm (clinical type probe)
• Target probing force should not exceed 20-25 g
• Division of the dentition into 6 sextants.
• All teeth are examined except the third molars (unless the first and/or second molars are
missing)
• If there are no teeth in the sextant its recorded as a cross
• If only one tooth present its included to the adjacent sextant
• Walking the probe around the entire gingival margin within each sextant, at least six points for
each tooth.
• For each sextant only the highest score/code is recorded.
• Should not be used around implants
• Radiographs should be taken for all code 3 and 4 sextants
Codes:

Interpretation of codes:

When to record:
• All new patients
• For patients code 0,1,2 the BPE should be recorded every routine examination
• For code 3 and 4 more detailed periodontal charting needed
• Code 3: initial therapy (OHI and risk factor control , then, post-initial therapy, record a 6-point
pocket chart in that sextant only.)
• Code 4: record a 6-point pocket chart for the entire dentition.

Advantages of BPE screening Examination:

• Simple and rapid screening system

• Well recognized internationally which aids communication of information
 56
• Encourages the examination of periodontal tissues in general practice (undiagnosed
periodontal disease is one of the major causes of litigation in dentistry)
• The system summarizes the periodontal condition
• Gives indication of treatment appropriate to the codes and suggests weather referral should be
considered
• Cost effective

Disadvantages and limitations of BPE:

• Lack of details within the sextants: (no. of affected sites or the severity)
• Lack of information on disease activity: (signs of bleeding on probing is referred to in only tow
codes 0 = not present, 1= present, does not account for amount of bleeding, site and delayed
bleeding)
• Inability to provide information about clinical attachment loss or plaque levels: (the codes are
based purely on the pocket depth, with exception to code * which implies the presence of
furcation involvement)
• Inability to differentiate between true and false pockets
• Lack of details about furcation involvement (which tooth is involved, which site and the
severity)
• Can not be used to monitor disease or response to therapy: (lack of detailed information within
each sextants)

❖ Must be done for every new patient, Provided that the limitations are understood and the scores are
carefully interpreted.
A simple and quick way of assessing whether significant periodontal disease is present and if so it
recommends a detailed examination
The BPE scores should be considered together with other factors when making decisions

Comprehensive periodontal exam:

• Pocket depth
• Clinical attachment loss
• Bleeding on probing
• Plaque index
• Gingival condition
• Suppuration (pus)
• Gingival recession (Classification of recession by Miller)
• Tooth mobility (Degrees of mobility by Miller)
• Furcation involvement ( Grades by Lindle and Nyman)
• Radiographic assessment

Bleeding on probing:
(Lang et al. 1990):
• The positive predictive value for disease progression was only 6%
• The negative predictive value was 98%
Thereby, the continuous absence of BOP is a reliable predictor for the maintenance of periodontal
health.

(Lang et al. 1986):

• The results indicated that pockets with a probing depth of 5 mm had a significantly higher
incidence of BOP.
• Patients with 16% or more BOP sites had a higher chance of loosing attachment.
 57
• Pockets with an incidence of BOP of 4/4 had a 30% chance of loosing attachment.
Therefore, Sites that remain BOP (+) may require re-treatment in most cases depending on no. of sites
and the incidence of BOP (+) in each maintenance visits and the level of plaque control as well as the
risk.

(Claffey et al. 1990): Diagnostic predictability of scores of plaque, bleeding, suppuration and
probing depth for probing attachment loss:
• After a few years of maintenance, increase in probing depth, particularly if combined with high
frequency of bleeding on probing, showed the highest predictive value for probing attachment
loss.
• BS 20-30% increased risk of attachment loss
• High frequency of residual deep pockets high risk for disease progression (Badersten et al .
1990)

Diagnosis: Current Classification System: (Armitage 1999)

I Gingival Diseases
II Chronic Periodontitis
III Aggressive Periodontitis
IV Periodontitis as a manifestation of systemic disease
V Necrotising periodontal disease
VI Periodontitis associated with endo lesions
VII Developmental / acquired conditions

Plaque index:
▪ The plaque index (Silness & Löe 1964 ) has possible scores of 0, 1, 2 or 3.
▪ The plaque control record (O’Leary et al., 1972) was developed to give a simple method of
recording the presence of the plaque on individual tooth surfaces (4) using disclosing.

Question 17: What does non-surgical periodontal therapy involve and when do we do RSD, why
and what instruments are used, what is supportive periodontal care, comment on the use of
local delivery antibiotics in periodontal disease. List the conditions where systemic antibiotics
are indicated?
 58
Aim of periodontal therapy: The control of the sub and supragingival biofilm to prevent further
attachment loss and preserve a functional and aesthetic dentition
• Disruption of the biofilm is the overall objective of professional debridement not the removal
of calculus
• Remove subgingival deposits
• Facilitate supragingival plaque control
• Allow tissue healing
• Reduce pocket depths
• Improve attachment level
• Prevent recolonisation

Treatment models for Periodontitis:

1- Infection model: Traditional treatment approach:
• Remove calculus as a source of infection
• Root plane ‘infected’ cementum
• Remove ‘infected’ bone
• Pocket surgery
2- Inflammation model: Disrupt the biofilm

Initial phase of periodontal therapy: Cause Related Therapy:

• Non surgical therapy
• Risk Factor Control Phase (OHI, removal of plaque retentive factors, smoking cessation,
manage of systemic disease, dietary advice)
• Plaque control phase
• Gingival phase
• Extractions, caries control, endodontic Tx., interim prosthetic replacement
Secondary phase: Corrective therapy:
• Surgical therapy
• Definitive restorative treatment
• Aesthetic treatment
Third phase: Supportive phase (Maintenance): To control further attachment loss
• Frequent and regular reassessment
• Monitoring and reinforcement of OH
• Professional cleaning

Control of biofilm:
Supragingival
Patient education, motivation, OHI, reinforcement, S&P + antimicrobials
Subgingival
Instrumentation + antimicrobials
Polishing: Removal of soft deposits and stain
• Difficult to reach interproximal areas
• Extends 2-3 mm subgingivally
• Achieves the same as GOOD PATIENT OH
• Removes aesthetically /socially unacceptable stain
• Alters bacterial load/composition

Scaling: The physical removal of surface deposits in readily accessible areas

Root surface debridement: subgingival scaling= deep scaling \Removal of all surface deposits in
subgingival areas including the root surface denuded of attachment beneath the soft tissues
o Less readily accessible areas
 59
o Remember subgingival doesn’t always mean on the root surface
o Supragingival scaling is always done at the same time
o The aim should be to disrupt all exogenous microbial deposits and produce a hard smooth root
surface less likely to harbour residual bacteria and cause persistent subgingival inflammation
o REDUCE THE BACTERIAL LOAD DISRUPT THE BIOFILM
o Disruption of biofilm Removal of all clinically detectable deposits With Hand or Ultrasonic
instruments
o When?
Presence true pocket 5mm+
After control of the risk factors
PS/BS no greater than 20%
Watch out however for location of the OH problem it may be in areas you intend to do the RSD even
if the overall score is 20%
After smoking cessation

Root planning: Previously thought to be essential if subgingival inflammation persists

• True pockets >4mm
• Removal of
• Root surface deposits
• Pathologically altered cementum
• Smoothing of the root surface

Instrumentation:
o Hand
Gracey curettes, which are site specific instruments
There are seven mirror image pairs of curettes in a full set.
GRACEY
Site specific instruments have only ONE CURETTE
cutting edge
INSTRUMENT COLOUR TEETH SURFACE
NUMBER

GRACEY 1/2 PINK UPPER AND ALL SURFACES

LOWER
ANTERIOR TEETH 15/16 mesial surfaces like
11/12
GRACEY 7/8 GREEN PREMOLAR AND ALL SURFACES
MOLAR TEETH BUCCAL/
LINGUAL ON
MOLARS
17/18 distal surfaces like
GRACEY ORANGE MOLAR TEETH MESIAL SURFACE
CAN BE USED ON 13/14
11/12 PREMOLAR

GRACEY BLUE AS ABOVE DISTAL SURFACE

13/14

o Sonic scaler: converts air pressure to vibrate (2-6 kHz) they have no effect on pacemakers
o Ultrasonic scaler: electric energy to mechanical energy (18- 45 kHz)
Mechanical disruption tooth surface deposits, irrigation and cavitation. The ultrasonic
scaler has the advantage of flushing away debris from within the pocket and introducing
an “ oxygenating” effect which will impact on anaerobic bacteria within the pocket

Types:
▪ Magnetostrictive units: electrical energy is applied to the coil generating magnetic
energy→ this applied to stacked metal strips crating mechanical energy→
elliptical stroke (all 4 surfaces moving → thus 4 active surfaces)
 60
▪Piezoelectric units: electrical energy is applied to the ceramic crystals
generating mechanical energy. → linear stroke→ lateral movement (thus lateral
surface is active)
o Tow principles of MOA:
▪ Cavitation: bubbles implode releasing energy→ enhance biofilm removal →
potential to disrupts bacterial cell walls.
▪ Acoustic microstreaming: forceful flow of cavitating fluid→ enhances
effectiveness beyond surface actually touched by the tip.
o Advantages:
▪ Quick
▪ Less tiring
▪ Good on mobile teeth
▪ Easier for cleaning furcation areas
▪ Useful for severe inflammation and haemorrhage
▪ Specific acute periodontal infections
▪ Good for stain removal

o Disadvantages:
▪ Loss of tactile sensation
▪ High powered suction required
▪ Some patients find it painful
▪ Some patients may complain of post-op sensitivity
▪ Can damage cementum (though less than hand scaling)

o Considerations:
▪ Cardiac pacemakers (implanted electronic devices) – although piezo electrics
thought to be safe? Not allowed at CDH
▪ Renal dialysis patients if using “ polyjet” Due to increased salt content.
▪ Dysphagia patients.
▪ Osseo integrated implants. (Cavitron have recently developed a new tip to
accommodate implants with a plastic protected tip)
▪ Severe respiratory diseases eg: Chronic obstructive airway disease
▪ May need to ask patients to turn hearing aids off due to whistling.
▪ Cochlear implants – vibration of machine can be painful?
▪ Patient’s fitted with brain stimulator (sometimes used in Parkinson’s disease).
Seek advice from neurosurgeon.

Barriers to instrumentation or reasons of Tx. failure:

▪ Operator skill: Poor dexterity of the operator, knowledge of anatomy
• Blunt and/or inappropriate instruments, wrong choice of currettes
• Roots morphology: teeth may be grooved making them difficult to instrument effectively
• Access: to posterior teeth, particularly the interdental areas pose barriers to effective
subgingival instrumentation, mouth opening, vision
• The deeper the pocket the more difficult it is to carryout subgingival instrumentation
• Patient tolerance

After non-surgical management → Re-assessment:

If successful outcome: patient put into supportive care
If unfavourable outcome: determine the reason

The 3rd World Workshop of the American Academy of Periodontology (1989) renamed maintenance
phase to “supportive periodontal therapy” (SPT).
This term expresses the essential need for therapeutic measures to support the patient’s own efforts
to control periodontitis.
 61

Effect of local antibiotic delivery:

The use of antimicrobials in periodontology, started due to the assumption that chemical aids
would compensate for technical limitations, and prevent early microbial recolonization to ultimately
ensure the best chance for clinical improvements.

Advantages of Local antibiotics:

• Delivered directly to the infected pockets
• Higher concentrations in the infected areas
• Reduces possible systemic side effects
• Doesn’t depend on the patient compliance
• Can be used in cases of peri-implantitis
• AAP recommends it’s use in case of more than 5 mm PD with inflammation after conventional
therapy.

Disadvantages:
• GCF washes any non binding drug placed in the pocket within 1 minute
• Can’t be used in cases where the disease in widely spread
• So far no local formula proved to be equally efficient or better than systemic combination of
amoxicillin and metronidazole
• Systemic antimicrobials are more cost effective (expensive)
• It delays the formation of junctional epithelium where it’s placed

Products available:
➢ Tetracycline in non resorbable plastic co polymer: Monolithic fiber packed in the sulcus, Better PD,
BoP and CAL
➢ Minocycline ointment and microspheres: The result of different studies showed improved PD but not
BoP / CAL (Hard to make it reach the base of the pocket since it’s viscous) (Matesanz-Pe´rez, 2013)
➢ Doxycycline in biodegradable polymer: Comes in two syringe mixing system, Better PD but not BoP/
CAL (Matesanz-Pe´rez, 2013)
➢ Metronidazole gel: Placed with a syringe in the pocket and it’s viscosity increase afterwards, better PD
and BoP but not CAL, Conflicting results in the literature (Matesanz-Pe´rez, 2013)
➢ Chlorhexidine products (Perio- chip): Gelatin chips (bovine Source), varnish, xanthan gels and
irrigation. No statistical significance was found for it’s use (Cosyn, 2006) , (Hanes, 2003)
➢ Azithromycin Gel: Only one study investigated it’s use and showed positive results (Pradeep, 2008)

Although many studies showed statistically significant level of PD reduction and CAL gain with
the use of adjunct antibiotics two questions remain:
• Whether such improvements, even if statistically significant, are clinically meaningful→ No
proof on the benefit of local type in the long term
• Do they justify the added effort and the likely added costs. (Very expensive)

(Bonito, 2005)

Systemic antibiotics in periodontology:

Used for Patients who: (Position Paper on systematic antibiotics in periodontology, by the AAP 2004)
• Aggressive type of periodontitis
• Acute periodontal infection e.g. periodontal abscess, acute necrotizing gingivitis/ periodontitis.
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Limitations:
• Pathogens involved in periodontal disease are many and differ in their sensitivity to
antimicrobial drugs
• Combination of antibiotics might be necessary to eliminate all of them
• Risk of developing antibiotic resistant bacteria
• Studies show that the biofilm prevents the antibiotic from reaching the bacteria

Combination antibiotic therapy:

• No single drug can cover all the Periodontal pathogens
• Antibiotic susceptibility test must be done before using them
• Metronidazole with amoxicillin ( perio pill) , Augmentin or ciprofloxacin gives synergistic
effect against mixed infections.
• An antagonistic effect might occurs, between bacteriostatic tetracyclines and other
bactericidal antibiotics (Winkelhoff, 1996)
Antibiotics prescribed:
• Doxycycline: 20mg/ twice daily (sub therapeutic dose) in chronic periodontitis treatment, in smokers
and non smokers population (clinical benefit in both smokers and non-smokers with CP.) (Preshaw,
2005)
• Metronidazole: 250 mg three times daily for a week Used in treatment of Necrotizing Ulcerative
Gingivitis (Johnson 1985)
• Amoxicillin can be used in the management of localized / generalized aggressive periodontitis
• Augmentin can be used for localized aggressive or chronic periodontitis that is not responding to
conventional treatment.
• Azithromycin is active against anaerobes and gram negative bacilli, Single dose of 250 mg/day for 5
days, after initial loading dose of 500 mg. Used for aggressive periodontitis and for reducing gingival
enlargement

Question 18: define gingival recession; mention common risk factors for it and classifications
and management:

Gingival recession: characterized by the displacement of the location of marginal periodontal tissues
apical to the cemento-enamel junction (American Academy of Periodontology 2001)
 63

Classification of gingival recession: (Miller, 1985):

Predisposing factors for recession:

1- Anatomical: (tooth position, crowding, displacement of tooth out of arch, bulbous root structure, enamel
pearls.)
2- Quantity of attached gingiva: inadequate is less than 2mm of AG (AAP, 2009)
3- Gingival biotype: a thin tissue biotype as a thickness of < 1.5 mm and a thick tissue biotype as a tissue
thickness > 2 mm (Claffey & Shanley 1986 ).however recent studies find it unrelated.
4- Bone morphology: gingival recession is often accompanied by alveolar bone dehiscence, although it is
not clear whether the underlying bone dehiscence develops before, or in parallel with gingival recession.
5- Malocclusion: Angle’s class II division II malocclusion have been associated with direct trauma on the
labial gingival margins of lower incisors and palatal of upper. A deep overbite in the absence of
adequate over jet may also lead to the stripping of the gingival margins. Severe class III malocclusions
combined with a deep bite.
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6- High attachment of fraenum: According to Chapple & Hamburger (2006) , contrary to popular
belief, there is no evidence in the published literature for a direct effect from so-called “fraenal pull” in
the initiation of gingival recession as the fraenum rarely has any muscle fibres.

Precipitating factors for gingival recession: there are a number of factors that may contribute to
the onset of gingival recession (Marini et al. 2004):

1- Plaque, calculus and periodontal diseases: either generalized recession in active or past
periodontitis patients, or localized plaque-induced inflammatory lesion.
2- Toothbrush trauma: usually located at buccal surfaces of canines, premolars and molars, associated
with wedge-shaped hard tissue.
3- Tooth movement: Labial tooth movement may result either from occlusal trauma accompanied by
periodontal diseases or from orthodontic movement. (If outside the bone envelope)
4- Smoking:
a. Systemically compromising the innate and adaptive immune response and
b. Topically reduced tissue vascularity influencing any subsequent wound healing of the
affected tissues.
5- Healing after periodontal therapy: in NSPT and ST (Lindhe & Nyman 1980)
6- Restorative treatment: Subgingival and overhanging restoration margins.
7- Removable partial dentures: poorly designed removable partial dentures may traumatize the
periodontal tissues either physically or as a result of plaque accumulation.
8- Self-inflected trauma/ chemical trauma: finger nail picking at the gingival margin, or lip and
tongue piercing have been reported to cause localized gingival recession, topical cocaine application.

Management of recession:
1- Preventive care: measurement and diagnosis, NSPT, OHI, diet advice, identify and correct the cause, ,
ortho tx. To correct misalignment, restorative correction of fixed or removable.
2- Non-surgical correction of the defects: use of gingival mask, tooth-coloured composite
3- Surgical correction:
▪ Pedicle soft tissue grafts; the laterally positioned pedicle graft and (ii) the coronally advanced
flap often used with enamel matrix derivatives, connective tissue graft or acellular dermal
matrix allograft material, depending on the amount of remaining keratinised tissue.
▪ Free soft tissue grafts: epithelial (free gingival grafts or (ii) subepithelial connective tissue
grafts.
▪ Guided tissue regeneration: using resorbable or non-resorbable membranes with or without
enamel matrix derivatives.

According to Miller (1985) complete root coverage can be anticipated in Miller class I and II
recession defects, whereas only partial root coverage can be expected when part of the interproximal
tissue is lost (Miller class III). Root coverage is not predictable in Miller class IV.

Question: 19: Mention tooth mobility classification and causes of mobility?

Miller (1950) , which identifies four degrees of movement:

▪ Degree 0 – “physiological” mobility; the tooth can be moved 0.1–0.2 mm in a horizontal direction
 65
▪ Degree I – the tooth can be moved between 0.2 and 1 mm in a horizontal plane (bucco-lingual or
mesio-distal direction).
▪ Degree 2 – the tooth can be moved 1–2 mm in a horizontal plane but there is no mobility in a vertical
plane (occluso-apical direction).
▪ Degree 3 – the tooth can be moved in excess of 2 mm in a horizontal plane and/or mobility in the
vertical direction.

Causes of pathologic tooth mobility can be due to one or more of the following:
1- Loss of tooth bone support: depends on the severity and distribution of bone loss, the length
and shape of the root, root size. However, the severity of mobility does not necessarily
correspond to amount of bone loss.
2- Trauma: due dental trauma to excessive occlusal force (luxation, root fractures), or abnormal
occlusal habits (bruxism), or trauma from occlusion
3- Extension of inflammation: from gingiva (periodontal dx.) or periapical dx. (dental abscesses
into the PDL. (Acute apical abscess)
4- Periodontal surgery: temporarily increases tooth mobility immediately after the intervention
and for a short period.
5- Pregnancy and menstrual cycle or contraceptives (physiochemical changes in the tissues)
6- Pathologic process: osteomyelitis, tumors of the jaws can destroy alveolar bone and roots of
teeth.

Question 20: Define the biologic width and what is the significance of it?

The biologic width (2mm) is the combined attachment width from the base of the sulcus to the
underlying alveolar bone, comprised of junctional epithelial attachment (0.97mm) and connective
 66
tissue attachment (1.07mm). However BW varies by location, gingival morphotype and study
methodology and can range from (0.75→4.3mm). (Gargiulo et al. 1961, Vacek et al. 1994). This can
be assessed by probing to bone level (sounding) under LA and subtracting the sulcus depth.

From a periodontal point of view both supragingival and equigingival margins are well tolerated.
The greatest biologic risk occurs when placing subgingival margins:

(Lang et al. 1983): 9 dental students with clean teeth and clinically healthy gingivae gave their
consent to participate in the study. 5 MOD cast gold onlays with 1 mm proximal overhanging margins
were placed in mandibular molars for 19-27 weeks: a subgingival flora was detected which closely
resembled that of chronic periodontitis. Increased proportions of Gram-negative anaerobic bacteria,
black-pigmented Bacteraides and an increased anaerobe: facultative ratio were noted. Following the
placement of the restorations with clinically perfect margins, a microflora characteristic for gingival health
or initial gingivitis was observed.

Restoration may need to be extended gingivally for:

1. Creating adequate resistance and retentive form in the preparation
2. To make significant alterations because of caries or fractures or restorations
3. To mask the tooth/restoration interface

When the restoration is placed too far below the gingival tissues it impinges on the gingival
attachment apparatus and violate the biologic width. The responses for that can be:
1. Bone loss of an unpredictable nature along with recession as the body defence creates space
between the restoration margin and the alveolar bone to allow for tissue reattachment, this is
more likely to occur in areas where the alveolar bone is very thin. Other factors that may
impact the likelihood of recession are: if the gingiva is thick and fibrotic or thin and fragile,
whether the periodontuim is highly scalloped or flat (highly scalloped and thin gingiva are
more likely to recede)
2. Gingival inflammation develops and persists without changes in bone levels.

To restore or maintain gingival health, the BW should be maintained by either crown lengthening
procedure or orthodontic extrusion.

Question 21: Define both aggressive periodontitis and ANUG and mention their clinical
manifestations and management?
 67
Aggressive periodontitis: differs from chronic periodontitis primarily by the rapid rate of disease
progression seen in otherwise healthy individuals and absence of plaque and calculus and a family
history of aggressive disease, can be localized or generalized.

Clinical features:
• Amounts of microbial deposits are inconsistent with the severity of periodontal tissue destruction and
• The progression of attachment and bone loss may be self-arresting.
• Absence systemic conditions
• Rapid attachment loss and bone destruction
• Familial aggregation
• Localised AP:
o Prevalence <1% (Caucasians <0.1-0.2, African American 2.6%)
o Usually has a circumpubertal onset
o Periodontal damage being localized to permanent first molars and incisors.
o Atypical patterns of affected teeth are possible.
o Frequently associated with Agribacter actinomycetemcomitans
o Neutrophil function abnormalities.
o A robust serum antibody response to infecting agents is frequently detected.
o Local factors inconsistent with tissue destruction
o Often absence or low levels gingival inflammation
• Genralised AP:
o Prevalence 0.13% (US national survey of adolescence)
o Onset usually under 30 years of age, but patients may be older. (10-30)
o There is generalized interproximal attachment loss affecting at least 3 permanent teeth other
than first molars and incisors. (More than 15 teeth)
o Attachment loss occurs in pronounced episodic periods of destruction.
o The disease is frequently associated with the periodontal pathogens Agribacter
actinomycetemcomitans and Porphyromonas gingivalis
o Neutrophil function abnormalities (hypoimmune neutrophil function and hyperimmune
macrophage function)
o A poor serum antibody response to infecting agents is frequently detected.
• Etiology: more than 90% of cases associated with Aa, elevated serum antibodies to Aa, Aa levels
decrease with successful therapy persist in unsuccessful cases

Treatment objective:
 Control risk factors for periodontitis, thereby arresting the progression of disease and thereby
maintain a functional and aesthetic dentition
 In addition, regeneration of the periodontal attachment apparatus where possible.

Management of AP: (AAP, 2004)

 Refer to specialist
 Initial NSM (Sc/RSD)
 Repeated with systemic antimicrobials (at first appointment) if patient compliant and initial
therapy unsuccessful.
 Perio pill (Metronidazole 250mg tds, and amoxicillin 500mg tds) if allergic to penicillin →
ciprofloxacin 500mg 2/day. If pt. is not complaint → doxycycline 100mg once a day.

Necrotizing periodontal diseases:

 68
Necrotizing ulcerative gingivitis (NUG) has a fusiform-spirochaetal microbial aetiology and is
more generally found in patients in developing countries who typically exhibit various risk factors,
including smoking, immunosuppression, in particular HIV positive status, stress, malnourishment
and poor diet. Key diagnostic features include:
• Pain
• Necrosis of the interdental papillae which have a “punched out” appearance, ulceration and spontaneous
bleeding
• Secondary foetor oris
• Pseudomembrane may be present
• May manifest in teenagers
• May progress to necrotizing ulcerative periodontitis (NUP).
NUG is the only form of gingivitis for which systemic antibiotics may normally be indicated as
part of the treatment. It is sometimes seen in children.

Necrotizing ulcerative periodontitis (NUP) Although not common in young people in developed
countries like the UK, necrotizing ulcerative periodontitis (NUP):
• May be an extension of NUG
• Features necrosis of the gingival tissues, periodontal ligament and bone, deep interdental osseous craters
• More cases of NUP are being described in immunocompromised patients esp. (HIV) or (AIDS)

Etiology: fusiform –spirochete bacterial flora + host factors

Management:
NUG→ treatment should involve elevation of acute symptoms and the correction of the underlying
chronic gingival disease.
1. Reduction of microbial load and removal of necrotic tissues (supragingival scaling an cotton swap to
remove pseudomembrane + CHX MW twice a day)
2. Pts with moderate to severe NUG and local lymphadenopathy or systemic signs are placed on
antibiotics (amoxicillin 500mg every 6 h for 10 days) if allergic (erythromycin 500mg every 6h) or
(metronidazole 500mg twice a day for 7 days) + analgesics for pain relieve
3. Review in 2 days and 5 days to continue Sc/RSD and evaluate symptoms and response to Tx.

NUP→ therapy includes local debridement, Sc/RSD, in-Office irrigation with CHX or Betadine,
meticulous OH, home use of M. In severe forms of NUP antibiotics may be prescribed. Prescription of
Metronidazole.(250 mg 2 tablets immediately and 2 tablets every 6 h for 5-7 days).

Caution in prescriping antibiotics for HIV patient, to avoid serious local candidiasis or even
candida septicemia → may need to prescribe prophylactic topical or systemic antifungal agent.

Question 22: List causes of gingival overgrowth and how to manage the condition:
 69
“Gingival overgrowth” is generally regarded as being related to an altered production of the
cellular components of the tissue, in particular the fibroblasts. the non-inflammatory components of
the process, although inflammation of the disordered tissue may well accompany the cellular
irregularities.
Can be:
Hypertrophic: A non-tumourous enlargement of an organ or a tissue as a result of an increase in the size
rather than the number of constituent cells.
Hyperplastic: “An abnormal increase in the number of cells in an organ or a tissue with consequent
enlargement”. Of Any cell type: epithelium, fibroblasts (most common in gingival tissues), myoblasts.

To achieve such changes in cell activity, a stimulus is required, which may be in the form of:
Drugs:
• Phenytoin (Dilantin, Epanutin), incidence 50%
o For treatment of epileptic conditions
o Use has declined in recent years, as other medication has been introduced (e.g.
phenobarbitone and carbamazepine) but when used in combination with these other anti-
convulsants the overgrowth is likely to be greater also used prophylactically in the prevention
of post-neurosurgical seizures.

• Cyclosporin (incidence 27%)

o immunosuppressant used in anti-rejection treatment for transplant patients
o It may also be used in the treatment of: diabetes, Bechet’s syndrome, multiple sclerosis,
systemic lupus erythematosus, erosive lichen planus.

• Calcium channel blockers (e.g. nifedipine, amlodipine, diltiazem) (Incedince 20%)

o Blood pressure regulators used as vasodilators in angina and hypertension

Hormones: This is plaque-related and the female hormones during:

o Pregnancy, oestrogen in particular, can be responsible for inducing:
▪ An altered microcirculation (from increased progesterone) and an altered sub-gingival
microflora from the second to eight months of pregnancy, allowing gingival fragility,
increased bleeding and an enhanced reaction to the plaque – “pregnancy gingivitis”
▪ Specific localised gingival overgrowth “pregnancy epulis”
o Genralised plaque- related enlargement and gingival fragility
▪ Puberty
▪ Oral contraception (OC)
▪ Hormone replacement therapy (HRT)
▪ Any situation where disturbed levels of progesterone/oestrogen is found, such as ovarian
disease.

Diabetes: Periodontal diseases in the presence of unstable diabetes may be associated with an
exaggerated response to the plaque resulting in an overgrowth of inflammatory origin, which is often
referred to as “hyperplastic gingivitis”.

Genetic influences: hereditary gingiva- fibromatosis, Individual fibromas

Neoplasms:
▪ Very rare but squamous cell carcinoma may present as unexplained gingival enlargement w/o
ulcerations.
▪ The overgrowth in leukaemic patients is associated with both the dense infiltration of white blood cells
into the tissue: (acute onset of gingival enlargement)

Other unusual conditions, which have been associated with gingival overgrowth include:
▪ Mouth breathing: enlargement of the upper labial gingiva in the presence of minimal plaque
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▪ Down’s syndrome: thick fibrous gingiva may obstruct OH
▪ Wegner’s granulomatosis, described as “strawberry gingivae”
▪ Sarcoidosis
▪ Crohn’s disease
▪ Scurvy – vitamin C deficiency
▪ Acromegaly.

Management:
Management of the overgrowth will depend upon the underlying cause and the clinical significance,
considering the following:
▪ How obstructive or disfiguring are the tissues?
▪ Is there restriction of normal function by gross enlargement?
▪ Is changing the medication realistic or possible?

Three basic modalities:

1. Conventional non-surgical periodontal therapy: with meticulous personal and professional plaque
control: to reduce the inflammatory component: NSPT, CHX MW
2. Surgical reduction of the overgrowth: accompanied by meticulous personal and professional plaque
control: This can be done as a gingivectomy, using:
▪ Incisional surgery
▪ Electro-surgery (diathermy)
o These approaches leave a painful raw surface and a protective periodontal dressing may
be required for 7–10 days
o The final shape of the healed tissue may prove unpredictable, especially if the medication
remains unchanged: Studies have reported as many as 34% of patients requiring repeated
surgical intervention.
3. Change in medication: with meticulous personal and professional plaque control. It may be that
alternative medications have already been tried and found less effective.

Question 23: Mention the prevalence of partial dentate population and RPD, indications,
consequences, free end saddle problems and hoe to manage them. Outcome of RPD treatment,
and describe features of swing lock RPD and when to use it, the use of sectional dentures?
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The prevalence of partial edentulism estimated greater than 20% (Cooper, 2009).
Results of the 1998 UK Dental health Survey indicates that the cut-off points at 21-24 teeth and
people with 21 or more are unlikely to have RPD:
• 21-24 teeth → 19% wearing RPD
• 15-20 teeth → 55% wearing RPD
The UK 2009 Dental Health Survey found that nearly one in five adults wore dentures (13%partial or
6%complete).

Removable partial denture is indicated in:

• Multiple missing teeth
• Long edentulous span
• No abutment posterior to the edentulous site (free end saddle)
• Excessive bone loss in the residual ridge
• Immediate or provisional restoration. e.g., patient transition to complete denture

Advantages of RPD:
• Minimally invasive treatment
• The ability to restore missing teeth and supporting structures
• Mask lost gingivae and provide lip support
• Distribution of occlusal forces: Teeth and mucosa
• Lower cost

Disadvantages
• Increased plaque retention:(Addy & Bates 1979) 45 pts. With dentures not performing OH for 3 days
only water rinse→ and plaque disclosing after that showd that:
o The wearing of RPD resulted in a significant increase in plaque accumulation found on both
buccal and lingual surfaces of the remaining teeth.
o In 10 pts. It caused plaque increase in the opposing arch
o The ligual plate showed significant more plaque than lingual bar
o Pts wearing the RPD day and night more plaque than day only
• Trauma from denture components
• Patient acceptance: Fixed vs removable
• Decreased patient tolerance due to Inappropriate design

Types Based on support, Beckett’s classification:

i. Tooth borne
ii. Tissue (Mucosa) borne
iii. Tooth and tissue borne

Types based on saddle area, Kennedy classification:

I. Bilateral free-end saddle
II. Unilateral free-end saddle
III. Posterior bounded saddle
IV. Anterior bounded saddle (crossing the mid-line)

Design steps:
Study models articulated and surveyed (Favorable path of insertion, Favorable & unfavorable
undercuts, Guide planes):
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• Outline the saddle area
• Support →rest seats = the resistance against movement of the saddle towards the ridge.
• Retention (direct)
• Reciprocation
• Major connectors
• Indirect retention: resistance against rotational forces on a saddle.
• Review and simplify

Clasps:
• Flexible component of a partial denture, which engages an undercut relative to the path of insertion.
Can be occlusal approaching or gingivall approaching
• The deeper the undercut the more flexible the material used to avoid lateral movement.
• Elastic modulus (rigidity)→ the higher th elastic modules the more rigid the material is:
o Co/Cr elastic modulus= 240 gPa → for a smaller undercut 0.25mm
o SS elastic modulus= 200 gPa → 0.5 mm undercut
o Gold elastic modulus = 75-100 gPa→ for deeper undercuts 0.75 mm undercut
• Selection of clasp depends on location of undercuts and abutment periodontal support
• Not recommended to use the Co-Cr occlusally approaching clasps on premolars since they are too
short to be flexible.

Every Denture principles: First introduced by Every in 1949 and include: (Australian dental
journal)
• Point contact with teeth proximal to the saddle(s) [bonded saddles].
• Minimum of 3mm gingival clearance.
• Mucosa borne Upper partial denture.
• Fully extended labial flange
• Path of insertion parallel to anterior ridge.
• Distal stops (wires)→For retention and to prevent backward drifting of posterior teeth.

How to manage difficulties in free end saddles?

The saddle of RPD is retained at one end only→rocking + insufficient retention.

Support is more of a problem due to the difference in displacement ability between abutment teeth
and denture bearing mucosa when loaded
• The periodontal ligament allows 0.1mm intrusion of the tooth
• Mucosa can be compressed by up to 2mm.
• Mainly in the mandible as the hard palate can compensate in the maxilla.

Routine methods for reducing the load:

➢ Wide tissue coverage of the saddle base to spread the load (buccul shelf, retromolar pad and lingual
sulcus)
➢ Reduction in the occlusal table by using narrow or less teeth.
Potential to torque and damage the abutment tooth with conventional RPD design.

1- RPI described by Krol : clasp that allows stress release

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Aims to bring axis of rotation anterior to clasp tip →bearing mucosa displaced under load →I-bar
and guide plate move away and disengage from tooth →avoid torque on abutment and tilting

R [Mesial rest seat]:

➢ Provide support against vertical loading.
➢ Prevent torque of abutment by directing ‘tipping’ forces towards the mesial surface.
P.S: The abutment tooth is usually supported on the mesial side by adjacent teeth.
Mesio-lingual minor connector reciprocate clasp action along with the guide plate.

P [Guide plane]:
➢ Provides bracing to RPD, distal proximal plate.
➢ Provides reciprocation to the abutment tooth against the clasp action.
➢ The proximal plate superior edge contacts the guiding plane at the junction occlusal and middle third
of the tooth, the undercut beneath the guiding plane allows release of proximal plate under load.

I [I-bar]:
➢ Provides direct retention when RPD rotate away from ridge.
➢ The approaching arm should be 3mm away from the gingiva, the bar approaching vertically and
2mm contact with tooth.
➢ Should be placed either mid-buccal or mesio-buccal, but not distal→ the I bar upon loading will
move in forward direction so if it was placed distally it will torque the tooth.
➢ Disengaged when RPD displaced towards the ridge.

Contraindications for use of RPI:

• Inadequate sulcus depth for I-bar (3mm)
• Severe lingual or buccal tilt of the abutment
• Severe tissue undercut → clasp will accumulate plaque and irritate the cheeks
• When lingual plate is used on the abutment due to shallow sulcus depth
• Only distobuccal undercut present

2- Altered cast technique (ACT):

• Two-stage impression technique for tooth and tissue borne RPD (mainly mandibular).
• First descried by Applegate in 1954 to cater for both supporting elements, reduced the potential for
occlusal errors and facilitated maintenance of the completed partial denture.
• End result is to record the tissue of free end saddle in a compressed/displaced state → reducing the
amount of displacement difference between the supported teeth and soft tissue under the saddle.
Sequence of procedure:
o Low viscosity overall impression is recorded (ZOE type II, light body PVS).
o Following metal try-in, a trial acrylic base is attached to the cast framework to be placed on the saddle.
o A wash impression is recorded only for the free end saddle
• Impression materials that can be used; Wax, compound, zinc oxide/eugenol paste, light or
medium bodied silicone.
• During taking the impression, pressure should only be applied on tooth-supported
• Components of the framework.
o Saddle area of the original cast is then replaced with new displacement version.
o RPD is processed on the new altered cast.
Evidence for success of altered cast technique:
(Leupold et al. 1992): This study clinically compared the vertical displacement of distal-extension
removable partial dentures made from different impression techniques (N=7). The impressions studied
were the altered-cast impression, an impression made from a border-molded custom tray, and a stock
tray irreversible hydrocolloid impression that served as a control. In each of these segments were two
adjustable measuring screws. The posterior screw served as a loading device and was located a
standardized distance from the terminal abutment.
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Results:
• Exhibited significance (p < 0.01) between the two impression techniques after intraoral loading was
performed. Although statistically significant, the 0.19 mm difference between the impression
techniques may or may not be clinically relevant.
• Control= 1.5 mm vertical displacement, ACT= 0.6mm, border molded technique =0.75mm

(Frank et al. 2004): RCT compared ACT to one-piece cast in Seventy-two patients receiving a
mandibular bilateral distal extension removable partial denture. Evaluated extension, support, and
adaptation of the denture bases by observation of border length and lifting of the indirect retainer from
its seat. The space between the soft tissues and the base when the framework was related to the teeth was
measured cross-sectionally at half the length of the denture base. Mobility, gingival index, and sulcus
depths at 6 locations around each abutment tooth were recorded at insertion and again 1 year later.
Results:
• The altered cast impression procedure does not offer significant advantages over the one-piece
cast, provided the standards used in this study are met. These include a completely extended
impression, use of magnification to adjust and ensure complete seating of the framework, and
coverage of the retromolar pad and buccal shelf by the base.

Other options for free-end saddle:

• Avoid RPD in mandibular free end saddle [Shortened dental arch].
• Distal cantilevered bridge→higher patient satisfaction. Contraindicated for RCTed abutment due to
rotating effect on the tooth causing oblique fractures.
• Dental implants→can be used as single tooth replacement, implant retained bridge, attachment system or
distal abutment (bonded saddle).
• Flexible joints [stress breaker]→ To join and separate the tooth and tissue components during loading→
Risk of fracture and fatigue + difficult to control and repair.

Swing lock RPD:

• Used when conventional denture design fails, It distributes the stress to all the remaining teeth and
ridges
• Indications: (Becker & Bolder, 1981)
o Bilateral free end saddle remaining teeth (C-C)
o Insufficient dental or alveolar undercut to retain conventional
o Missing or weakened abutment teeth, or periodontally compromised
o Poor tooth support due to pattern of tooth loss
o Hemi-maxillectomy or mandibular resection
• Requirements:
o 6-8 mm sulcus depth
o Good OH, sufficient manual dexterity
o Low lip line
• Framework features:
o Bar spanning for minimum length 4 teeth for flexibility
o Reciprocation from palatal plate
o Direct retention from small vertical struts (similar to I-bars)
o Arc of closure free of interferences
o The hinge might be placed in the sulcus instead of distal edge of last standing tooth if interferences
present
Sectional dentures:
• Is a prosthesis which is composed of tow or more parts each utilizing different path of insertion
• They are used to exploit undercuts around teeth, hard and soft tissues, which require more than one
path of insertion (typical trapezoid shaped edentulous space.
• Anterior saddle → use of splint pins
• Posterior saddle→ oblique cut and magnets
• Advantages:
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o Improve aesthetics (eliminates black triangles and removal of clasps in some situations)
o Improve retention (in severe undercut areas)
o Eliminate food traps interproximally in tilted teeth
o Increase stability
• Disadvantages:
o Highly skilled dentist / technician
o High pt. dexterity
o Regular maintenance (pins and bolts for reactivation)
o Mechanical detrition or biological adaptation may allow the denture to be removed as a
whole unit

Outcome studies in RPD:

(Carlsson et al. 1965): longitudinal clinical follow-up study of 99 patients with RPD. (11 drop-outs)
• They divided the sample to 5 groups (G1-pt. with lower PD, G2-Pt. with upper PD, G3-Pt. didn’t
wear their dentures, G4-pt. lower PD with bilateral free-end saddle, G5-Pt. Pt. with change in
denture status)
• Denture wearing: 15 pt. did not use their dentures.
• Mobility: 18% abutment teeth became loose after 4 –years, 25% increased mobility
• Caries in abutments: in G4→ 41 out of 44 of abutments without crown were carious, other groups 43
out of 74 abutments. For the crowned teeth only 2 out of 53 crowned abutment. Control (5 out of 28)
• Occlusion deteriorated in all cases with time

(Tada, 2013): tooth loss in RPD patients (147):

• 5 yr. survival rate of direct abutments was 87%, indirect abutments 93%, lower than non abutments
96%
• Abutment survival rate was associated with possible, risk factors for tooth loss:
o C:R ratio
o Root canal Tx.
o Pocket depth >5mm
o Type of abutments
o Occlusal support (one zone in contact, (Eichner Index)→so more teeth lost the higher the risk
of losing more teeth.

(Tada, 2014): periodontal maintenance impact on tooth survival in RPD pts.(192 pt.) (cohort study)
• 3 groups: 3-6 months, 1 yr, and no maintenance.
• 7-yr cumulative survival rate was: 84%, 76%, 72% of abutments
• At least 2-yr maintenance is recommended.

(Kapur, 1994): RCT compared RPI design to circumfential clasp design with distal rest for 5-yrs.
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• In Kennedy CI and CII showed: 71% success rate for circumfential, 76.6% SR for RPI not
significant difference.
• Success= no failed abutment (loss or mobility >G3), pt. wears the denture during eating.
• Well-constructed removable partial denture of either design, supported by favourable abutments and
accompanied by a regular recall (6-month) program offers a satisfactory treatment modality.

(Jepson, 2001): RCT (Newcastle study) 30 pts. with mandibular shortened dental arch allocated to 2
groups randomly: (1) received RPD, (2) bilateral cantilever RBB. They were examined at 6months, 1
year, and 2yrs for caries incidence.
• 20 out of 27 of the bridge pts. And only 9/23 denture pts. Had no caries experience
• Most RPDs had lingual plate with gingival coverage
• The relative risk of caries was 4 times more in dentures compared to bridge group
• Most of caries were root caries.

(Carreiro et al. 2016): assessed periodontal conditions of abutments vs. non-abutments in RPD pts. (22)
after 7 years of use:
• Higher gingival recession and probing depths indexes found on direct abutments.
• Direct abutment exhibited more (33%) caries and fractures
• The lack of periodontal maintenance during the 7-years may justify the results

(Preshaw et al. 2011): literature review on the impact of RPD on oral and systemic health, concluded:
• There is clear evidence that the RPDs increase plaque and gingivitis, particularly on abutment teeth.
• There is no clear evidence for increase risk of periodontitis
• The risk of caries (root caries) appears higher.
• Regular recall should be part of the treatment.
• There is no evidence to support a negative impact of RPDs on nutritional status or general health.

Question 23: Explain the Dental Practicality Index –assessing the restorability of teeth by
(Dawood & Patel, 2017):

Aims:
• Assist the clinician in deciding when to seek advice and/or refer a patient for secondary or tertiary dental
care.
• Aid in the systematic assessment of dental restorative problems
• Enhance communication between collaborating practitioners
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• Help to manage patient expectations before carrying out restorative treatment

Features:
• Each of the restorative categories; structural integrity, periodontal state and endodontic state are
assessed and weighted according to their current state and the complexity of potential treatment.
• The context: this category relates to the oral environment, the patient’s ability to maintain their
dentition (local context), and the practicality of restorative treatment in the context of ‘the bigger
picture’. Taking into account not only their overall restorative needs, but also the impact of treatment
in the wider context of their social, dental, and medical history (general context) must be taken.

After a comprehensive assessment of the patient, the DPI score is derived by adding together the
scores allocated in each of the four previously described categories.
• An overall DPI score of 1–2 implies that if there is a periodontal, endodontic, and/or structural issue that may be simply
and predictably treated.
• Level 2 score is recorded for any one of the restorative categories, advanced training and expertise in managing complex
problems would be desirable; these cases may be referred for secondary or tertiary care.
• A DPI score ≥6 suggests that it is not practical to carry out definitive treatment to a tooth and other treatment modalities
such as an implant might be considered

Question 24: List reasons of tooth loss and effects of tooth loss?

According to the WHO In 2015, Global life expectancy at birth was 71.4 years (73.8 years for females
and 69.1 years for males). Global average life expectancy increased by 5 years between 2000 and
2015:
• There is a documented decline in edentulism in the literature
• The mean number of lost teeth increases with age
• Total tooth loss can be also related to social class and marital status
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• Most complete denture treatment will be centred on old people; likely to become more complex and
demanding

Risk factors for tooth loss:

• Caries
• Periodontal disease
• Trauma
• Pain due endodontic and periapical disease
• Orthodontic reasons

Effects of tooth loss (edentulisum):

• Psychological effects:
o Difficulties in accepting the loss of their teeth
o Some patients take more than a year to get over the loss
o Feelings of sadness, anger and depression
o The feeling of getting prematurely old
o Loss of confidence which negatively affects relationships with others
o Limitations in food choices and enjoyment
o Limit social participation
• Biological effects:
o Loss of the area of the periodontium that supported masticatory load on the tooth→Thus, a 75%
quantitative deficit in supporting tissues occurs after extraction
o Low biting load for mucosally borne dentures
o Mastication inefficiency (Watt & MacGregor 1986)
o Loss of bone surrounding the roots of lost teeth→Loss in height and buccal contour of the ridge
▪ Maxilla loses around 2.5 mm of ridge height and 2-3 mm of buccal contour after a year of
extraction (Carlsson et al. 1967)
▪ Immediate denture wearers tend to lose less bone (Statically insignificant)
▪ The hard palate remains unaffected by the resorption
▪ Mandible loses around 4-5 mm of ridge height and 3.6 mm of buccal contour after a year
of extraction (Carlsson and Persson 1967)
▪ The mean reduction in height of the mandibular region was 4 times greater than maxilla
(Tallgren 1967)
o Loss of support for the facial muscles;
▪ Shortening of the buccinator muscle
▪ Decrease in cross-sectional areas of masseter and medial ptergoid muscles (esp. in older
patients)
▪ Decrease in the density and loss of tone of the facial muscles
o Loss of lip and cheek support

Question 25: list the different types of dentures and mention indications for transitional
dentures, advantages and disadvantages, different ways to transition to edentulous:

Types of dentures for transition to conventional complete dentures:

1. Transitional dentures:
• Indications:
o Transition to edentulous when anticipating problems in adaptation or tolerance to
complete dentures →Training period allows the patient to develop denture control
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o Can perform any adjustments needed to provide comfort and function before
extraction of remaining teeth
o As a temporary option in young pt. until fixed or implant placed
o For wear cases to replace missing teeth and establish stable occlusion at an acceptable
OVD.
o Prolonged restorative tx. or periodontal tx. It is used to maintain function and aesthetics.
o Pediatric pt. in case of severe hypodontia and pt. growing.
• Advantages:
o Simple, economic, allows adaptation
o Maintain function and appearance
o Can use information given by remaining teeth
• Disadvantages:
o Repeated addition to the denture may be inconvenient for the pt.
o Problems can arise from the remaining teeth at any time
o Prolonged tx.
o Position of remaining teeth may be unacceptable.
o If it was poorly fitting or incorrect occlusion, the pt. may be discouraged to wear it and
may compromise the future denture adaptation.

2. Overdenture (described in details previously)

3. Immediate dentures:
• Advantages:
o Maintenance of dental appearance and facial contour
o Minimizing disturbances of mastication and speech
o Easier adaptation to dentures than leaving the arch edentulous for months
o Maintains patient’s physical and mental well-being
o If patient’s existing jaw relationship was acceptable, this can be transferred to the
immediate denture→ to avoid guess work
o The form and relation of the natural teeth can be reproduced if the pt. likes their
appearance.
o Reduction in ridge resorption – evidence is inconclusive
o Haemostasis: supports and protects the clot post extraction→ Provides “protective
bandage” for surgically traumatized area
• Disadvantages:
o Inability to complete a comprehensive trial stage
o Increased maintenance; the need to reline the denture after the extractions
o Short service life; will not last as long as a conventional denture due to the morphological
changes in the oral environment
• Contraindications:
o Patients at risk from bacteraemia? controversial
o Previous history of post-extraction hemorrhage
o Presence of gross oral sepsis: pt. who neglected their mouth → surface deposits, caries
and gingival inflammation → pt. may be less concerned about appearance anyway.

4- The clearance with no immediate removable denture:

• Advantages:
o Allows period of healing and initial alveolar modeling
o The delay of taking impressions allows more stable supporting areas for the denture
o The denture will retain their fit for a longer period
• Disadvantages:
o Loss of masticatory function and appearance during healing period
o Undesirable mental and physical effects
o Tongue spread and cheeks may invade future denture space
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o Difficult to assess vertical/horizontal relationships for new dentures

Question 26: explain stability, retention and support in complete dentures, define combination
syndrome and list its features, how to manage flabby ridge. And list the different impression
techniques. Explain technique to manage unstable mandibular denture?

To achieve denture stability:

• Retentive forces acting on the denture > Displacing forces
• When the dentures have adequate Support

Retention: resistance to vertical movement of the denture away from the underlying mucosa.
The retentive forces that act on the dentures are of two main types:
1. (Muscular forces):
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• Forces exerted by the muscles of the lips cheeks and tongue upon the polished surface
• Muscles of mastication indirectly through the occlusal surface
• Successful muscular control depends on the denture design and patient’s skill
2. (Physical forces):
• Forces that rely on the presence of intact film of saliva between the denture and the mucosa
• Dependant on the maintenance of a seal between the mucosa and the border regions of the denture
and the accuracy of fit.
• Surface forces (Adhesion): Attraction forces between saliva and the acrylic resin or the saliva and
mucosa
• Fluid forces (Cohesion): Attraction forces between the saliva molecules
• Atmospheric pressure: Resists displacing forces on the denture provided there is an intact peripheral
seal.
• For optimal physical retention:
o Border seal and peripheral seal: create a post-dam by cutting a groove in the working cast
normally at the vibrating line. Or by using mucocompressive impression technique to
displace the mucosa in the post-dam area
o Area of impression surface “maximum coverage”: use as much as possible of denture
bearing area.
o Accuracy of fit

Support: Determined by the form and consistency of the denture bearing area
• Alveolar ridge (resorbed or not, Flabby ridge)
• Hard palate
A reduction in support promotes instability → if the ridges are resorbed:
• Resistance to lateral displacing forces will be poor
• Occlusal contacts produces tipping with the denture pivoting about the mid-line of the palate

The denture bearing area:

The combination syndrome: (Lynch, 2004)

First described by (Ellsworth Kelly, 1972), as changes caused by mandibular RPD apposed by upper
complete denture.
The prevalence of flabby ridges can vary, occurring in up to 24% of edentate maxillae and in 5% of
edentate mandibles. Such flabby tissues could also arise as a result of unplanned or uncontrolled
dental extractions.

Clinical Features:
• Resorption of the max. Labial plate leading to flabby ridge
• Overgrowth of the maxillary tuberosity
• Papillary hyperplasia of the hard palate (not always)
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• Extrusion of the lower anterior teeth
• Resorption of mandibular bone under the partial denture bases (if worn) posterior saddle area.

Potential problems:
• Inter-ridge discrepancies (this is more exaggerated when opposing natural teeth to produce a
satisfactory occlusion)
• Flabby anterior ridge which compromises support (thought to be caused by differential forces on
an edentulous ridge caused by a partially dentate opposing arch)
• Enlarged tuberosity limits correct occlusal plane orientation and space for artificial teeth

Kelly proposed that this scenario was caused by what is commonly termed insufficient ‘posterior
occlusal support’, leading to increased occlusal forces on the anterior part of the maxillary complete
denture by remaining anterior natural teeth. These forces led to resorption of the maxillary labial
plate, and subsequent ‘tipping’ downwards of the posterior section of the maxillary complete
denture into which the tuberosities enlarged due to ‘negative pressure.

Management:
• Recognition of abnormal oral anatomy (upper flabby ridge);
• Identification of the necessity of specialized impression technique;
• ‘Early’ assessment of stability/retention/fit of complete denture by fabricating a heat-cured transparent
baseplate prior to occlusal registration;
• Selection of shallow-angled cusped teeth;
• Face-bow transfer – particularly useful in this case, allowing suitable orientation of the occlusal plane,
and locating the arc of closure nearer to the hinge axis, reducing the likelihood of a premature contact;
• Arrangement of teeth on a semi-adjustable articulator to ensure balanced articulation.
• A magnetic retention system is a useful adjunct where ‘conventional’ retention is not readily available.

All impressions for complete dentures could be categorized in three ways:

1- The mucostatic technique: records the un-displaced denture bearing areas at rest. The denture adapt to
tissues at rest has good retention but forces wont be distributed evenly on the underlying tissues.
2- The mucocompressive technique: compresses the tissues the same way the denture does and so more
distribution of forces.
3- The selective pressure impression technique-where some denture bearing tissues are displaced, and
others are not. Which is the most impression techniques used for conventional dentures. If close-fitting
custom trays and high viscosity impression materials are used, the soft tissues at the vibrating line on the
palate are compressed, while the tightly bound mucosa on the hard palate is not.

There is no evidence to indicate that one technique produces better long-term results than the other.

For the flabby ridge:

1- An impression technique is required which will compress the non-flabby tissues to obtain
optimal support, and, at the same time, will not displace the flabby tissues → because if the flabby
tissues are compressed during the impression they will recoil and dislodge the resulting denture.

Techniques suggested: (Lynch, 2006)

Liddlelow→ described a technique whereby two separate impression materials are used in a custom
tray (using ‘plaster of Paris’ over the flabby tissues, and zinc oxide and eugenol over the ‘normal’
tissues).
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Osborne→ described a technique whereby two separate impression trays and materials are used
to separately record the ‘flabby’ and ‘normal’ tissues, and then related intra-orally.

Watson→ described the ‘window’ impression technique where a custom tray is made with a window
or opening over the (usually anterior) flabby tissues. A mucocompressive impression is first made of
the normal tissues using the custom tray and zinc oxide and eugenol. Once set, it is removed, trimmed,
and re-seated in the mouth. A low viscosity mix of ‘plaster of Paris’ is then painted onto the flabby
tissues through the window. Once set, the entire impression is removed.

Watt and McGregor→ described a technique where impression compound is applied to a modified
custom tray (3 sheets of wax spacer over the flabby tissue area, one sheet for the remaining areas).
The thermoplastic properties of this material are then manipulated to simultaneously compress the
‘normal tissues’, while avoiding displacement of the ‘flabby tissues’ using the same material and
impression tray. Over this manipulated impression compound, a wash impression with with zinc-
oxide and eugenol is made.

‘Newer’, more ‘easy-to-use’ materials, such as polyvinylsiloxanes (silicones) can also be used. By using
putty for compressive and light body PVS for the static.

2- other treatment modalities include:

• Surgical ‘debulking’ or excision of the flabby tissues:
o Not for pts. with medical problems for which surgery is contraindicated.
o The excision of flabby tissues and resultant ‘shallow’ ridge may provide little retention or resistance
to lateral forces on the resultant denture.
• The use of dental implants:
o May need bone grafting due to excessive ridge resorption (questionable prognosis)
o Medical conditions unsuited to have implants
o Pt. preference of not having invasive surgical procedures.

How to manage unstable mandibular denture: (Lynch, 2006)

An unstable mandibular denture can be due to:

• Incorrect extension of buccal or lingual flanges
• Poorly adapted fitting surface
• An atrophic mandibular ridge
• An inappropriately contoured polished surface or positioning of the teeth
• Diminished or altered neuromuscular control (Parkinson’s dx., stroke)
• Surgical resection

The “neutral zone” or “denture space” is zone of minimal conflict between buccal (cheeks and lips)
and lingual (tongue) musculature within a denture should be situated.
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The denture should be countoured so that it doesn’t encroach on this space during function→ if it
does the forces will result in displacement of the denture.
The artificial teeth should occupy the same positions as their natural predecessors.

In some patients this space has been limited as a result of poorly planned transition to edentulous
state. Uncontrolled tooth extraction can lead to:
• Lateral spreading of the tongue in the posterior part of the mouth
• Excessive anterior resorption leading to increased prominence of the mentalis muscle.
In other pts. The shape of the zone is bizarre due to surgical resection, stroke, scleroderma or a
prominent mental groove.

How to record the neutral zone:

Neutral zone impression:

Indication:
When there are particular problems in achieving stability of a lower denture
• Highly atrophic mandible
• Abnormal muscular activity
And the pt. cant place implants due to medical conditions or finances.
A denture shaped by the neutral zone (NZ) technique will ensure that the muscular forces are working
more effectively and in harmony.

Advantages:
• Improved stability and retention
• Posterior teeth will be correctly positioned allowing sufficient tongue space
• Reduced food trapping adjacent to the molar teeth
• Good aesthetics due to facial support

Procedure:
• Carried out after the stage of recording the occlusion and articulation.
• Removal of the wax from the lower base plate and construction of a superstructure (vertical wire
loops) that can provide even occlusal stops at the correct OVD and to provide support for the NZ
impression material.
• Ensure that the structure does not deflect the cheeks, lip or tongue and that the desired OVD is
maintained
• With the base plate out of the mouth place the correct volume of a high viscosity mix of tissue
conditioner (viscogel soft liner) on the superstructure, mould it into a rim and place it in the patient’s
mouth.

• Instruct the patient to perform repeated actions:

o Swallow and take frequent sips of water
o Talk aloud, pronouncing the vowels and count from 60 to 70
o Smile, grin, lick their lips and purse their lips
• These actions will mould the material by muscle activity After 10-30 minutes, when the impression
has set, remove the plate and proceed to the laboratory stage.
• The lab will construct a plaster index which they can use to set the lower teeth according to
 85

Question 27: Explain the copy denture technique in terms of indications, advantages and
clinical steps:

Copy dentures; copies the tooth positions and polished surfaces of the existing dentures whilst
improving the fitting surface to compensate for resorption of the residual alveolar ridges
• Minor modifications can be made
• Care must be taken with the occlusal vertical dimension

Indications:
• Duplicate set of dentures (Spare dentures)
 86
• Where minor corrections are required, but where the dentures are largely satisfactory
• Successful immediate dentures where the original natural tooth positions were copied
• Patients who would have difficulty in accommodating changes to their dentures→ the patient will have
become accustomed to the shape of the prostheses, and have developed muscular control accordingly
• Elderly patients where their learning ability has diminished
• The duplicate denture can serve as an impression tray; a surgical guide, or it can be used for research
purposes.

Contraindications:
• Failed dentures
• Very old and worn dentures
• Copies of copies

Clinical steps:
• Take an impression of the existing denture (Can be done with alginate and a dupe box or using Lab putty
and stock trays)
• Pour wax until the level of gingival margin and denture base poured with cold cure acrylic
• Record the occlusion
• Construct trial dentures and wax try-in stage + take a wash impression in the copy denture
• Finish and fit of dentures

Question 28: Mention the challenges in dealing pt. with severe gage reflux and list different
management techniques?

Gagging: is a protective reflux to stop unwanted entry of substances into the mouth and oropharynx.

Aitiology:
• Somatic: reflux triggered by tactile stimulation
• Psychogenic: arise fro sight, sound or thought as a result of bad past experience, or disturbing story or
psychological disturbances.
• Systemic: GI tract diseases eg: persistent gastritis
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Managing gagging pt. during impression taking:
1- Reassurance and relaxation
2- Position of the pt.: sitting upright
3- Breathing through the nose: slow, deep and even breathes
4- Close fitting custom tray: less bulky, start with lower impression, minimum amount of material, use
saliva ejector
5- Distraction: by talking, reinforcing breathing technique, ask pt. to raise one leg and not lowering it
until done.

The severe gagging pt. for denture wearing:

1- Training denture: new stimuli introduced gradually, the pt. has to cope with one small step at a
time. In a process called “Desensitization”.
• Impression with compound→ training bases constricted with posterior extension judged to be
appropriate (hourseshoe, palatless, to vibrating line)→ chair side reline
• The base should be worn as long as tolerated before gagging starts and then removed and rest
period and then worn again but increasing time. Repeat until successful.
• Further additions can be introduced: more extensions until a CD is provided
2- Relative analgesia: only for taking the impression.
3- Acupuncture: have been shown to be controlled
4- Hypnosis: for severe cases depends on pt. well motivated and open minded to the practice

Question 29: Define denture stomatitis and mention management?

Denture stomatitis: varies from patchy to diffuse inflammation of the mucosa covered by denture. It
may be associated with inflammatory palatal papillary hyperplasia and angular stomatitis. Usually
symptomless, pt. is unaware of it.
Types: classifies by Newton (1962):
1- Pinpoint hyperaemia
2- Diffuse inflammation
3- Granular
If microbiology confirmed candida → named “chronic atrophic candidiasis”
Prevelance: 10 – 60% of pts. wearing CD
 88

Aetiology:
Local factors:
• Presence of candida
• Trauma from the denture
• Poor denture hygiene: method of cleaning and storage
• Wearing denture at night
Systemic factors:
• Age: more common in elderly
• Gender: more common in females 4:1
• Immunological deficiencies
• Hormonal imbalances: diabetes
• Nutritional deficiencies (Vit B complex, Vit C and iron)
• High carb diet: increase candida growth and adhesion of microorganisms to denture
• Drugs causing dry mouth

Treatment:
1- Improve denture hygiene: lab cleaning of denture, daily brushing of denture with soap rinsing
before storage in disinfection of denture (overnight immersion in alkaline hypochlorite (0.08%
chlorine), aqeous CHX (0.1%)
2- Correction of denture faults: occlusal faults, impression surface faults→ soft lining
3- Leaving the denture out at night
4- Antifungal preparations: topical application (Mw, ontiment, iozenges) of Amphotericin B,
Nystatiin, Fluconazole to the denture and to the lesion. Recurrence after stopping them is high, so
denture hygiene instructions are more important.
The above measures will usually are effective in curing within 2-3 weeks if there are no underlying
systemic factors.
5- Systemic therapy: referral to medical practitioner for further investigations.

Question 28: Explain tooth wear process, prevalence, etiology, signs and symptoms, diagnosis
and prevention, management and outcome of treatment?
 89

• Eccles suggested that the term ‘tooth surface loss’ should be used when a single aetiological
factor was often difficult to identify. Loss of hard tissue surfaces of teeth, which occurs as a
result of a physical agent or chemical agent (Eccles 1982).

Smith and Knight, however, considered that ‘TSL’ belittled the severity of the problem and, therefore,
advocated the use of the term ‘tooth-wear’ to embrace all three aetiological conditions.

Prevalence:
▪ Systematic review on prevalence of tooth wear in adults reveled that the predicted percentage
of adults presenting with severe tooth wear increases from 3% at the age of 20 years to
17% at the age of 70 years. Increasing levels of tooth wear are significantly associated with
age.
(Spijker AV. et al. 2009)
▪ Systematic review of prevalence of tooth wear in children and adolescents, prevalence of
wear involving dentin ranged from 0 to 82%, in children up to 7 years and increased with
age, prevalence in adolescents range from 0 to 54%, age and wear were not related.
(Kreulen CM., Spijker AV. et al. 2010)

▪ The observational, cross-sectional study across seven European countries reported by

Bartlett et al. with the highest levels of tooth wear observed in the UK, where 54.4% of
participants scored BEWE 2 or 3.
o In the UK higher levels of BEWE grade 2 and 3 were present on the molars and premolars.
In other countries more typical distribution found in the anterior teeth.
o This study suggests that tooth wear is highly prevalent in Europeans, with nearly 30% of a
young adult population affected by tooth wear to a degree that may have important oral
health and health economic implications.
(Barttlet, 2014)

Although the actual prevalence of TSL is unclear, there is general agreement that the population,
particularly the young, is experiencing increased exposure to elements which cause TSL.

Signs and symptoms: (Wazani, Dodd & Milosevic, 2012)

From records of 290 pts. Presenting to Liverpool Uni. Dental hospital for tooth wear retrospectively:
• Significantly more males (56%) presented with severe tooth wear compared with females (31%)
• Aesthetic concerns were the most prevalent presenting complaint (59%).
• Sensitivity was the second most common presenting complaint (40%).
• Functional problems and pain were less prevalent at 17% and 14% respectively.
• Subjects who had lost posterior support had more severe wear and more worn anterior teeth,
which was statistically significant (p = 0.001).
• The proportion of subjects with undiagnosed apical pathology on worn teeth was 13%.

Abrasion: The pathological wearing away of dental hard tissue through abnormal mechanical
processes involving foreign objects or substances repeatedly introduced in the mouth and contacting
the teeth.
 90
• Energetic tooth brushing→More than 100 years of normal tooth brushing needs to remove
1mm of the hard. (Addy & Hunter, 2003)

Attrition: The physiological wearing a way of dental hard tissues through tooth-to-tooth contact,
without the intervention of foreign substances.
• Affect occlusal surfaces, incisal edges and proximal contacts.
• Characteristic features are antagonistic plane facets with sharp margins
• Causative factors:
o Stress related/ bruxism
o Lack of posterior support? (Smith and Robb 1996 + Systematic Review Van’t Spijker et al.
2007 → are not in support for it., Wazani et al. 2012+ Milosevic 2016 → support it)
o Congenital tooth abnormalities AI/DI. (Systematic review Poulsen et al. 2008, kim&Simmer
2007)
o Ecstacy. (Milosevic et al., 1999)

Abrafction: The wedge-shaped non-carious cervical lesions in the cemento-enamel junction area.
• Theory behind this lesion is explained by eccentric occlusal forces during horizontal movements of the
jaw. Loading of tooth cusps would cause tensile stress concentrations in the cervical region, leading to
micro-crack formation, particularly in the enamel, which resists tensile stress less well than dentine.
• Abfraction could be a stress-corrosion phenomena caused by a combination of high cervical stresses and
dietary acid. (Rees et al. 2003)
• The combined mechanisms of cyclic fatigue stress and biocorrosion could contribute to the formation of
NCCLs. (Grippo et al. 2013)

Erosion: The physical result of a pathologic, chronic localised loss of dental hard tissue that is caused
by an electrolytic or chemical mechanism, without bacterial involvement.
“Biocorrosion is the chemical, biochemical or electrochemical action which causes the molecular
degradation of the essential properties in a living tissue” is a more precise term than erosion. (Grippo
et al. 2012).
• Characteristic clinical features of erosion are loss of surface structure, melted appearance, cupping or
grooving on occlusal/incisal surfaces, and shallow concavities coronal from the cemento-enamel
junction.
Differences between erosion vs. caries:
• Surface: Dental erosion is the pathologic process which dental surface structures are
destroyed by the action of acid, without bacteria being involved. Dental erosion is often
described as a surface phenomenon, however, besides removal and softening of the surface,
dissolution of mineral underneath the surface occurs. In caries the destructive effects involve
both the surface and the subsurface region.

• Plaque: Unlike caries, the acid that cause erosion are not produced by the oral flora. Erosion
occurs in areas that are free from dental plaque.

• Critical PH: in caries its 5.5 and in erosion its 4.5

• Tooth erosion is an irreversible process and no remineralisation is possible due to lack of

matrix as a consequence of enamel loss. In contrast early diagnosis of caries will allow for
enamel remineralisation.

Pathogenesis and modifying factors of dental erosion:

• Erosion of enamel
• Erosion in dentine
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• Dentine hypersensitivity: Prevalence of 18.3% and 18.6% for sensitivity in patients with
moderate and severe tooth wear were respectively and 3.1% in the mild category (Wazani
et.al 2012). Different than DH not related to tooth wear reported by Rees et al. (2000) 3.8%.
• Critical pH value:
o The pH at which the fluid surrounding the solid tooth surface is just saturated with respect
to tooth mineral. Above this pH, tooth mineral will not dissolve; below this pH
demineralisation can occur.
o Teeth begin to dissolve when pH drops below 4.5
• Acids and chelating agents:
o Chemical erosion of the teeth occurs either by the hydrogen ion derived from acids, or by anions
which can bind or complex calcium and known as chelating agents.
o Citric acid: each acid anion has a different strength of calcium complexation. Citric acid has
double actions and is very damaging to the tooth surface.
• Buffering capacity:
o The ability of an acidic solution to dissolve enamel or dentine depends on its titratable
acidity or buffering capacity
o The greater the buffering capacity of the drink, the longer will it take for saliva to neutralise
the acid, and the more mineral may be dissolved before dissolution stops .
o It is measure by adding alkali solution at room temperature to the drink being tested (0.1M
sodium hydroxide), when the pH reached neutrality (pH of 7) the total volume of the alkali
required is the tritability of a drink.
o Higher Neutralisable acidity value means more ‘free’ acid.

• Acquired pellicle:
o It comprises mucins, proteins, glycoprotein, and several enzymes.
o Carbonic anhydrase VI enzyme helps to prevent erosion by accelerating the neutralisation
of the hydrogen ions on the surface layers of the teeth
o Salivary pellicle can partially protect against erosion challenges and also clears the erosion-
inducing acids from the surface

• Saliva: Protective mechanisms of saliva:

o Helps to dilute acids in the mouth
o Partly neutralise the acids in the oral fluid
o Slower dissolution rate of mineral due to the calcium and phosphate levels in the saliva
o Inhibits or slow down mineral loss during acid dissolution by salivary mucins and other
organic components from a pellicle
o Increased saliva production by the acid induced stimulation of the salivary gland.

Diagnosis:
(Smith & Knight, 1984): Tooth Wear Index:
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(Bartlett et al. 2008, 2010): Basic Erosive Wear Examination:

❑ Clinical examination
❑ High density stone study casts,
❑ Intra-oral photographs, intra-oral scanners
❑ Wear relative to age
❑ Salivary test.
❑ Radiographs: (periapical and bitewings) are important for assessment of thickness of
remaining enamel and dentine, as well as existing crown/root ratio and periapical
pathosis.

Causative factors of erosion:

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1. Extrinsic factors:
o Chemical factors
o Biological factors (saliva, acquired pellicle, tooth structure variations)
o Behavioural factors
o Environmental factors
o Medicaments

2. Intrinsic factors:
o Gastro-oesophageal reflux disease (GORD): hidden gastric reflux 40%
o Oesophageal symptoms o Extra-oesophageal symptoms
▪ Heartburn ▪ Retrosternal pain
▪ Epigastric pain ▪ Asthma
▪ Regurgitation ▪ Chronic cough and sore throat
▪ Dysphagia ▪ Hoarsness
▪ Globus
o Alcohol abuse
o Eating disorders:
o Anorexia o Bulimia
▪ Mainly females, Low self-image ▪ Mainly females, Low self-image
▪ Intelligent, Early adolescence ▪ Compulsive
▪ Dietary restriction ▪ Intelligent, Late adolescence
▪ Low body weight ▪ Binge/purging
▪ Low metabolic weight ▪ Normal body weight (± 15%)
▪ Minimal drug use ▪ Electrolyte imbalance
▪ Drug and alcohol abuse
o Rumination

Risk factors for erosion:

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(Jarvinen et al. 1991): Case control study, 106 cases with erosion and 100 randomly selected
controls from the same source population were involved in the study. All cases and controls were
evaluated by the recording of structured medical and dietary histories and by examination of the teeth
and saliva:

Consumption of citrus fruits more than

twice a day is the highest risk factor
For erosion (OR=37) followed by vomiting
weekly or more (OR=31).

Prevention:
– Early recognition
– Risk assessment
– Education
– Control of further tooth surface loss

Advice:
• Diet history (identify acidic vs. sugar)
• Low erosive drinks:
o Avoid drinks with citric acid
o Increasing the dilution factor of dilutable fruit drinks within a range likely to be acceptable
to the consumer may not effectively reduce their erosive potential.(Hunter, 2008)A
o All fruit teas are found to be highly acidic and able to remove the smear layer (Rees et al.
2006)
o Under highly controlled conditions the erosion of enamel by solutions of dietary acids is
influenced by the interplay of pH, acid concentration and presence of calcium. These variables
and in particular the concentration of calcium could be manipulated to produce soft drinks with
reduced erosivity to enamel. (Hughes et al. 2000)

• Daily fluoride: effects of topical fluoride:

o Topical fluoride does allow remineralisation of enamel which is beneficial in managing
erosion (but not as effective as in caries)
o Apply topical F on teeth affected by erosion at recall appointments
o Continue to recommend using F toothpastes and MW

• Tooth mousse/Pronamel: (Rees et al. 2007)

o Pronamel has increased levels of bioavailable fluoride
o Bioactive ingredient in Tooth Mousse is casein phosphopeptide. Casein based carrier is to
allow delivery of calcium and phosphate ions to the surface and maintain the necessary
concentration gradient to encourage remineralization.
o Amount of surface enamel erosion was reduced by 48% in the proenamel group and by 35% in
the tooth mousse group.
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• Tooth brushing before meals: Attin demonstrated in an in-situ study that abrasion resistance of
softened enamel increases with remineralization period and at least 60 min should elapse before
tooth brushing after an erosive attack

• Use of straw, cold drinks:

• Low abrasive toothpaste: tooth pastes need to be below 250 RDA to be safe (RDA=relative dentine
abrasivity).
• Milk or bicarbonate solution for gastric reflux
• Dentine bonding agents:
o (Azzopardi et al. 2004): 20 day study, Seal and Protect (a self-etching resin) and Solo
(partially filled resin that requires separate etching of the dentine). Both bonding agents
protected the teeth in this wear regime, Seal and Protect exhibiting more in vitro wear than
those coated with Solo.

o (Gwinnett and Jendresen) resin tag penetration into tubules of sclerotic dentine was observed
to be significantly less than in primary dentine.
Normal Dentine Sclerotic Dentine
Acid penetration 100 micro m 30 micro m
Resin bonding strengths 22-30 MPa 16-19 MPa

o (Sundaram et al.) showed the longevity of sealants in the form of dentine bonding agents applied to
teeth displaying severe wear to be relatively short lived, they may help to reduce the rate of wear on
applied surfaces by up to a period of nine months following application.

When to treat?
• Known risk factors have been minimised by dietary and behaviour modification
• No symptoms eg. dentine hypersensitivity
• Deteriorating appearance or chipping
• Continued loss of OVD
Restorative options:
• Composite build ups.
• Minimal preparation adhesive restorations ± Dahl approach
• Conventional fixed restorations
• Removable onlay/overlay prostheses
Properties of different restorative material: (Chu, dental update, 2002)
 96

Management options:
• Prepare teeth (+/- OVD): Pulpal vitality loss 10-15% (Cheung et al.)
• Orthodontics (+ prepare teeth)
• Surgical crown lengthening (+ prepare teeth)
97
 98
Outcome of treatment:

Composite in localised tooth wear (Anterior Dahl):

(Gulamali & Hemmings et al. 2011): 10- year procpective survival results of 283 anterior composite
Dahl restorations (direct, indirect and combination):
• 50% probability that composite Dahl’s will survive 7 yrs. 90% of composite Dahl’s showed
major/minor failure over 10 year.
• Survival analysis – The median survival time (MST) for all the restorations was 7 years considering
major failure mode only and combined major and minor failure levels the MST was 5 yrs and 9
months.
• 81% exhibit complete re-establishment of posterior occlusion with Shimstock foil .
• No significant difference between direct, indirect, or for the technique utilising the combination of
the materials.
• Common failure: Wear (45%)
o Marginal discolouration (28.9%)
o Fracture (21.6)
• Risk factors for failure Class I incisal relationship
o Abrasion
o Opposing ceramic surface
• With some degree of maintenance, repeated use of composite resin restorations to treat localised
anterior tooth wear at an increased occlusal vertical dimension is a viable treatment option over a
ten-year period (For short- to medium-term )
• The factors that significantly influenced the survival of restorations were the incisal relationship,
aetiology, material used, and the nature of opposing dentition

(Hemmings et al. 2000) Sixteen patients were restored with 104 restorations in 2 groups:
• Mean follow-up of 30 months has shown a combined success rate of 89.4% for both groups
with 93 of the restorations remaining in service
• Direct hybrid composite restorations with a dentine-bonding agent placed at an increased
vertical dimension of occlusion effectively treated localized anterior tooth wear.
• The occlusion was restored in 4 to 5 months, and maintenance was minimal over 30 months.
• Have shown favourable short- to medium-term performance of direct composite resin
restorations when placed in a thickness of 2 mm or more.

(Poyser et al. 2007): Prospective split-mouth clinical trial of 168 direct composite restorations in
18 patients. Restorations were placed on the mandibular anterior teeth to increase the anterior
OVD between 0.5 - 5 mm and were evaluated after 2.5 years:
• Complete failure occurred in 6% of the restorations.
• Circumferential preparation and height of the restorative addition did not influence the
performance of the restorations.
• The posterior occlusal contacts were restored after a mean duration of 6.2 months (range: 3–
13 months) in 14 out of the 15 ‘Dahl’ sub-group patients.
• Loss of restorative volume was due to wear rather than fractures.
• Marginal breakdown and staining were the most common form of deterioration of composite-
based restorations.
• Direct composite restorations placed at an increased OVD are a simple and time-efficient
method of managing the worn mandibular anterior dentition.
 99
(Al Jawad & Rees, 2016) Audit Sample 41 patients Mean age was 39.6 years (range 21 – 70 yrs)
Mean follow up 25 months:
• Major failure 4.4%
• Minor failure 8.7%

(Milosevic & Burnside, 2016): 1010 direct composite Dahl most of them in anterior teeth in 164
pts. a prospective 8-yr study:
• Over an average follow-up time of 33 months, only 71 (7%) of 1010 restorations in this sample
failed. (Failure was defined as a total debond or chip of composite)
• Failure higher in lower arch (9.6%) vs upper arch (6%)
• Failure higher with lack of posterior support and with attrition
• Bruxism and an increase in the occlusal vertical dimension were not associated with failure;
composites placed in attrition cases had the lowest survival.
• Lack of posterior support as defined by 6 or more pairs of missing posterior teeth (premolars
and/or molars) resulted in a significantly reduced survival
• The proportion of failures was greater in patients with a Class 3 or edge-to-edge incisal
relationship (but this was not statistically significant).
• To date, this study is the largest case series of patients with tooth wear restored with a single direct
composite resin placed by one operator.

(Ahmad & Murbay, 2016): Survival Rates Of Anterior Composites In Managing Tooth Wear:
Systematic Review:
• Three prospective and two retrospective studies were identified involving the placement of 772
direct and indirect anterior composite restorations in 100 patients, with a follow-up period between 5
months to 10 years.
• The results of included studies do support the use of anterior composites as a management modality
for tooth wear patients with favourable short/medium term survival rates of over 90% at two
and a half years and over 50% at 5 years.
• In regard to the success of increase in OVD in patients and re-establishment of posterior occlusion,
all studies reported an OVD increase between 0.5 and 5 mm, with a restoration of posterior
occlusion in 91% of cases (n = 91/100) within 18 months.

Composite in generalized tooth wear (Anterior & Posterior): most are case series:

(Attin et al, 2012): Case series of 6 patients, follow up 5.5 yrs:

• Some deterioration in marginal quality, discolouration and surface texture

(Redman, 2003) Composite resin restorations have the advantages of ease of repair or
modification. However, they still suffer from wear, margin staining, marginal fracture and surface
roughness.

(Schmidlin et al. 2009) case series, the authors conclude that direct resin composite materials
represent a viable economic method to restore severely worn posterior teeth at least for the
medium-term.

(Bartlett & Sundaram, 2006) An Up To 3-year Randomized Clinical Study Comparing Indirect
And Direct Resin Composites Used To Restore Worn Posterior Teeth:
• 32 paired restorations, in 16 pts. With severe tooth wear, 26 pairs of restoration in 13 pts without
tooth wear.
• Insufficient OVD was available → increased by 2-3 mm.
• No protective splint was given post-opt.
• Tooth wear due to combination of bruxism and erosion
 100
• For tooth wear group all restorations were restored at the retruded contact position
• In the tooth wear group: 50% of restorations were retained, 22% fractured, 28% lost.
• In the control group: 80% were retained, 4% fractured, 8% lost. (8% DNA)

• No statically significant difference in the outcome between the two materials within groups.
• Likely cause of high failure may be the high loading forces from bruxing actions and the impact of
increased OVD.
• Another possibility maybe the brittle physical properties of the microfilled composites
• What effect a Michigan or full coverage heat-cured acrylic resin splint worn at night, may have had
on the outcome is not possible to predict

Therefore, it appears that increasing the OVD by direct composite resin restorations is a predictable
medium-term option, while metal or ceramic onlays are more adequate as long-term options.

Gold Onlays:

(Chana et al. 2000) reported a 89% survival rate of resin bonded metal (Cast type III gold)
alloys veneers for a duration of 5 years. 12% of the restorations were cemented in supra-
occlusion as a one-stage Dahl procedure. no more prone to failure than those that were placed
following traditional inter-occlusal tooth preparation.

(Jamous et al. 2007) found that 80% of resin bonded metal restorations survived after seven
years.

Ceramic Onlays:

(Wagner et al. 2003) reported that the survival of ceramic onlays was 81% in seven years. (In the
same study, they found that the performance of ceramic onlays is comparable to metal onlays)
(Otto & Schneider 2008) found the survival rate for ceramic onlays to be 89% up to 17 years.

Question 29: briefly explain and mention success and survival rate of single crowns, FPDs, RBB
and veneers?
 101

Single crowns:

(Burke, 2005) 4-year Prospective evaluation of 59 dentine-bonded crowns placed in a dental

school environment for patients. 48 were available for examination and only Three crowns had
failed due to porcelain fractures, an overall failure rate of 6%.

(Pjetursson, 2007): systematic review of survival and complication rate of PFM and all ceramic
single crowns five- year survival estimates of:
• PFM → 95.6% for a mean follow-up of 9-years
• All ceramic (densely centred alumina)→ 96.4% for a mean of 4.5 years
• All ceramic (re-enforced glass ceramic) → 95.4% for a mean of 4.2
• All ceramic (glass ceramic) → 87.5% for a mean of 6.9
Conclusions:
• All-ceramic crowns, when used for anterior teeth, showed survival rates at 5 years comparable to
those seen for metal–ceramic crowns.
• When used for posterior teeth, the survival rates at 5 years of densely sintered alumina crowns
(94.9%) and reinforced glass–ceramic crowns (93.7%) were similar to those obtained for metal–
ceramic crowns.
• Lower survival rates of 90.4% and 84.4% can be expected for In-Ceram crowns and glass–
ceramic crowns when utilized for premolars and molars.

(Sailer & Pjetursson et al., 2015): systematic review of survival and complication rate of PFM
and all ceramic single crowns five- year survival estimates of:

• Cumulative 5 year complication rates:

• Caries on abutments: (0.5% -2.1%)
• Abutment tooth fracture: (0.1% -1.2%)
• Loss of abutment tooth vitality: (0.7%– 3.7%)
• Marginal discoloration: (1.8% - 8.3%)
• Framework fracture: (0.03% - 6.7%)
• Ceramic fractures: (0.3% -3.2%)
• Ceramic chipping: (1.2% 3.5%)

Fixed Partial Bridges (Conventional bridges):

(Schwartz et al. 1970), Unserviceable crowns and FPDs: after studying a group of 791 failed
restorations:
• The mean life span for all fixed prosthodontic restorations was 10.3 years.
• Canine to canine FPD has a life span of 15 years.
• Caries was the cause of 37% of the failures.

(Tan & Pjetursson et al., 2004): a systematic review of survival and success rates of FPDs:
 102
• 10 yr. survival for FPD was 89.1% while success was 71.1%
• 10 yr. risk for caries and periodontitis leading to FPD loss was 2.6% and 0.7%, respectively
• 10 yr. risk for loss of retention was 6.4%, for abutment fracture 2.1% and for material fractures 3.2%
• 10 yr. risk for loss of abutment vitality was 10%

(Pjetursson et al. 2007): a comparison of survival and complication rates of tooth-supported FPD,
and implant supported FPDs and single crowns:
• 5-year survival of conventional FDP was 93.8 %, which dropped to 89.2% after 10 years of
function.
• 5- year survival of cantilever FDPs of 91.4%, solely implant supported FDPs of 95.2%. At
10-year SR dropped to 80.3% for cantilever FDPs, to 86.7% for implant-supported FDPs.
• Most frequent complications were biological complications like caries and loss of pulp vitality

(Pjetursson et al. 2015): a systematic review of survival and success rate of multiple- unit FPDs:
• 5 year survival rate of metal-ceramic FDPs was 94.4%
• 5 year survival rate of reinforced glass ceramic FDPs was 89.1%
• 5 year survival rate of glass-infiltrated alumina FDPs was 86.2%
• 5 year survival rate of densely sintered zirconia FDPs was 90.4%
Biological complications:
• Secondary caries – Overall 5 year complication rate was 1.4%
• Loss of vitality – Overall 5 year complication rate was 2.2%
• Periodontal disease –2.9% to 7.6% at 5 years.
Technical complications:
• Framework fracture – highest failure rates was 8% for reinforced glass ceramic FDPs and
12.9% for glass infiltrated alumina, whereas, sintered zirconia exhibited highest stability as
framework material over 5 year.
• Ceramic fractures and chipping of ceramics were frequent

(Plamqvist & Swartz, 1993): artificial crowns and FPD 18 to 23 years after placement:
• The long-term results were good, especially for the MCC: 79% remained unchanged and only 3%
had been removed. The success rate for the gold-resin restorations was less favorable: 43% remained
unchanged and 33% had been removed.
• The use of one cantilever extension unit had not negatively influenced the results.

(Sailer et al., 2007): systematic review of survival rates of all ceramic FPDs compared to MCC:
• 5 –yr. survival estimates for MCC → 94.4% mean follow-up 8 yrs.
• 5-yr. survival estimate of all ceramic FPDs → 88.6% mean follow-up 3.8 yrs.
The frequencies of material fractures
• Framework and veneering material fracture were significantly higher for all-ceramic FDPs (6.5%
and 13.6%) compared with those of metal–ceramic FDPs (1.6% and 2.9%).
• If posterior teeth shall be replaced with an all-ceramic FDP, zirconia should be used as the
framework material. However, the veneering ceramics for this high-strength framework material
exhibit higher rates of chipping than the ones observed for metal frameworks.

(Burke, 2012): ten-year survival of bridges placed in general dental practice in UK:
• Data for over 80,000 different adult patients were analysed
• Conventional bridge abutments placed within the NHS Regulations in England and Wales have
demonstrated satisfactory longevity, at 72% without re-intervention at 10 years
• Factors significantly related to decreased bridge survival were type of bridge (resin-retained
performing less well than conventional), patients with high treatment need and patients who
changed dentist.
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(De Backer et al. 2008): up to 20-yrs. results of short vs. long –span FPDs:
• The overall survival estimations for Ss-FDPs (70.8%) and Ls-FDPs (52.8%) at year 20,
Difference were statistically significantly different.
• The reason for failure in the Ss-FDP group was of biologic origin in 55.6% to 66.7% of cases,
but for the Ls-FDP group the failures were of technical origin in 56.0% to 84.0% of cases.

(Balevi, 2008): Ante’s low revisited: They included in the review only studies of FDPs with
abutment teeth that did not meet the requirements of Ante’s low:
• A meta-analysis incorporating the results of only two studies yielded an estimated FDP
survival rate of 96.4% after five years and 92.9% after 10 years. These results were
comparable with published survival rates of FDPs with abutments that satisfied Ante’s law.
• The long-term prognosis of FDPs with abutments that have severely reduced periodontal
support depends on proper control of periodontal disease, strict adherence to a maintenance
care program and rigid splinting of mobile abutment teeth.

(Valderhaug et al. 1980): Recession after subgingival margin placement:

• 40% of margins become supragingival at 1 year
• 71% by 10 years

Resin bonded bridges:

(Creugers et al 1992) A seven-and-a-half-year survival study of resin-bonded bridges

• A clinical trial involving 203 resin-bonded bridges.
• Survival of anterior and posterior RBBs were 75% and 44% (respectively) after 7.5 years.
• The early ‘Rochette-bridges’ had a high rate of failure.
• RBBs made in patients with a 'deep-bite incisor relation were less retentive than RBBs in
patients with a 'normal incisal relation
• For anterior RBBs, maxillary RBBs were less retentive than mandibular RBB.

(DeKanter & Cragers, 1998): a 5-year multi practice clinical study on posterior RBB:
• The survival rate at 5-year for the posterior RBB in the maxilla (65%) was significantly higher
than in the mandible (40%).
• Preparation of grooves is beneficial.

So best prognosis for RBB is in anterior mandible, worst prognosis is for posterior mandible.

(DJEMAL, 1999) Long-term survival characteristics of 832 resin-retained bridges and splints
provided in a Eastman post-graduate teaching hospital:
• Un Perforated retainers, blasted with 50 micron alumina and luted with Panavia® Ex
• The median survival was 7 years and 10 months.
• The median survival for fixed-fixed designs was 7·8 years and is certainly significantly
shorter than the 9·8 years for the cantilever design.
• The postgraduate students experienced greater success than junior hospital staff.
• Increasing the surface area covered was a powerful factor tending to enhance survival.
• Debonding was the most common reason of failure.

(Chow, 2002): Hong Kong D- design preparation features for posterior RBB:
• The grooves on proximal and palatal/lingual surfaces of abutment teeth serve 2 main
functions: to define the path of insertion and to provide retention and resistance form to the
retainer against the dislodging forces acting on the pontic
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• Strut provides the restoration with rigidity and support by connecting the mesial and
distal rests
• Chamfer finish line

(Pjetursson et al 2008) A systematic review of the survival and complication rates of RBB after an
observation period of at least 5 years:
• Meta-analysis of 17 studies indicated an estimated survival of RBBs of 87.7% after 5 years.
• The most frequent complication was debonding, which occurred in 19.2%
• The annual debonding rate for RBBs placed on posterior teeth tended to be higher than
that for anterior-placed RBBs. This difference, however, did not reach statistical significance.

(King, 2015) Survival characteristics of 771 resin-retained bridges provided at a UK dental

teaching hospital:
• 80.8% the 5 year survival rate and 80.4% the 10 yr. survival rate.
• The majority of failures happened in the first 4 years and the most common reason was
debonding.
• The minimal or no preparation showed higher success than ones with preparation.
• Presence of restoration beneath the framework reduces the success rate three folds.
• The cantilever design showed higher success rate than fixed-fixed design due to the avoidance
of differential movement of the abutments teeth when fixed-fixed design is used.
• The experience of the operator had a major role with survival rate for staff and post grads over
double that of the inexperience undergraduate.
• Use of rubber dam did not make a difference.
• The use of a double-cantilevered bridge replacing upper lateral incisor teeth using both
centrals as the abutments is reported as a predictable option and may aid orthodontic
retention in situations where the central incisor teeth have been moved orthodontically→ the
failure rate of this type of restoration was 8.7% over a 15-year follow-up period.

Question 30: Mention quality assurance in dental radiology?

Quality Assurance (QA): Ensure consistently adequate diagnostic information whilst keeping doses
as low as practical. Should include:
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• Image quality
• X-ray equipment
• Darkroom, films, processing
• Training
• Audit

Why do QA?
The law now requires that anything which can potentially lead to extra irradiation of either patient,
staff or general public has to be meticulously monitored. For:
1. Perfect results every time
2. Reduced radiation dose (to ourselves)
3. Improved diagnostic quality
4. Reduced costs

Subjective quality ratings of radiographs:

1. Excellent- no errors of exposure, positioning or processing. (should be not less than 70%).
2. Acceptable- some errors which do not detract from the diagnostic use. Not greater than 20%.
3. Unacceptable- errors, which render the radiograph diagnostically unacceptable. Not greater than 10%

Routine tests are then carried out to monitor the performance of the equipment.
• In GDP, X-ray sets must be regularly checked for radiation safety at least once every 3 years.
• In hospitals it can be every year All X-ray equipment must be serviced according to the manufacturer’s
specification. This is usually annually. Includes automatic processors.

X-ray equipment check annual/3 yearly for GDP’s (Usually undertaken by RPA)
1. kV accuracy 5. Dose at end of collimator/dose width product
2. Exposure time accuracy Intraoral set DPT Equipment
3. Radiation output 6. Focal spot size
4. Accuracy of collimation/beam size 7. Mechanical safety

QA for radiographic technique: Appropriate training and instruction;

Intra-oral technique:
Use of film holders with beam aiming devices.
DPT:
Use light beam diaphragms for correct patient positioning.

Processing errors:
Dark films may be due to: Pale films may be due to:
- Over exposure - Under exposure
- Light fogging - Under development
- Over development - Excessive fixation

Before taking the radiograph?

1- Patient referral – is adequate clinical information available? (Justification, Pt. ID, clinician)
▪ Is radiograph necessary?
▪ Has the patient been correctly identified by 2 means?
▪ Check problem area with the patient
▪ Can less films be taken to give same information?
2. ID x 2 – do we have the correct patient? (Always double check)
3. Communication – do we understand each other’s objectives?
Question 31: Describe HIV dental aspects and how to manage pts. with HIV:
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Immunodeficiencies are states that result from a defect in the immune response, and predispose
to recurrent infections. Human immunodeficiency virus (HIV) disease and the resultant acquired
immune deficiency syndrome (AIDS) constitute a major immunodeficiency and public health issue.
• HIV infects CD4+ helper T lymphocytes, causing AIDS after an average of 10 years in the untreated
HIV transmission: Mostly via body fluids, Sexual intercourse (semen, blood and possibly saliva),
contaminated blood products and donated organs, contaminated needles, vertical transmission
(mother to child), during childbirth and via breast milk.
• HIV cannot reproduce outside the body and is not spread by air, water, insects, social contact, closed
mouth or social kissing, saliva, tears or sweat

DENTAL ASPECTS
• Factors increasing the potential for postoperative complications in HIV/AIDS – low CD4 count,
high viral load, low lymphocyte count, neutropenia, bleeding tendency, another concomintant
infection
• There is a theroretical interaction of LA with antiretroviral treatment
• Bleeding may be aggravated by NSAIDs such as aspirin; codeine and paracetamol are safe
analgesics but can interact some ART however it is insignificant clinically
• Oral candidosis common in 50% of patients – conventional antifungal treatment is indicated initially
• Association with ANUG

Question 32: Describe the association of Bisphosphonates and dentistry and what is MRONJ:
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The Scottish Dental Clinical Effectiveness Programme, March 2017:

Medication-related osteonecrosis of the jaw (MRONJ) is a rare side effect of anti-resorptive and
antiangiogenic drugs. It is defined as exposed bone, or bone that can be probed through an intraoral
or extraoral fistula, in the maxillofacial region that has persisted for more than eight weeks in
patients with a history of treatment with anti-resorptive or anti-angiogenic drugs, and where there
has been no history of radiation therapy to the jaw or no obvious metastatic disease to the jaws.

Symptoms:
Although the majority of cases of MRONJ occur following a dental intervention which impacts on bone,
some can occur spontaneously.
◦ Delayed healing following a dental extraction or other oral surgery,
◦ Pain, soft tissue infection and swelling, numbness,
◦ Paraesthesia or exposed bone.
◦ Pain or altered sensation in the absence of exposed bone.
◦ Some patients may be asymptomatic at presentation.

Pathophysiology:
Current hypotheses for the causes of necrosis include suppression of bone turnover, inhibition of
angiogenesis, and toxic effects on soft tissue, inflammation or infection. It is likely that the cause of the
disease is multi-factorial, with both genetic and immunological elements.

Risk factors:
◦ Underlying medical condition for which the patient is being treated, (cancer pts. +previous episode of
MRONJ)
◦ Cumulative drug dose (also linked to duration of drug treatment)→ pts. taking the drug for >5 yrs.
◦ Concurrent treatment with systemic glucocorticoids,
◦ Dentoalveolar surgery and mucosal trauma (procedure that impacts on bone, extractions)

Patient has taken bisphosphonate drugs in the past but is no longer taking them for whatever reason (i.e.
completed or discontinued the course or taking a drug holiday), they should be allocated to a risk group as if
they are still taking the drugs.
◦ The effect of denosumab on bone turnover diminishes within nine months of treatment completion.
◦ Anti-angiogenic drugs are not thought to remain in the body for extended periods of time
Incidence:
◦ In cancer patients approximates 1% (patients with prostate cancer or multiple myeloma to be at
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increased risk)
◦ In osteoporosis estimates range from 0 to 0.1%
◦ The incidence of MRONJ after tooth extraction is estimated to be 2.9% in patients with cancer and
0.15% in patients being treated for osteoporosis.

Medications:
There are two main types of anti-resorptive drugs that have been associated with osteonecrosis of
the jaw, the bisphosphonates and denosumab. These are used in the management of osteoporosis
and other nonmalignant and malignant conditions.

Bisphosphonates:
The bisphosphonates reduce bone resorption by inhibiting enzymes essential to the formation,
recruitment and function of osteoclasts. The drugs have a high affinity for hydroxyapatite and persist
in the skeletal tissue for a significant period of time, with alendronate having a half-life in bone of
around 10 years.
◦ They have an adverse effect on soft tissue cells by inhibiting proliferation and increasing apoptosis,
which may lead to delayed soft tissue healing.
◦ There is also some evidence that these drugs can inhibit angiogenesis.
Uses:
◦ To reduce the symptoms and complications of metastatic bone disease (particularly that associated
with breast cancer, prostate cancer and multiple myeloma). The drugs are usually delivered as
regular high dose intravenous infusions in this patient group.
◦ The treatment of osteoporosis.
◦ Paget’s disease, osteogenesis imperfecta and fibrous dysplasia.
◦ Prophylaxis to counteract the osteoporotic effects of glucocorticoids and to prevent bone-related/
skeletal complications in patients with primary hyperparathyroidism and cystic fibrosis.
◦ Patients in these groups can take the drugs orally (usually once a week) or the drugs can be given as
quarterly or yearly infusions.

Denosumab:
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A fully human monoclonal antibody which inhibits osteoclast function and associated bone
resorption by binding to the receptor activator nuclear factor κB ligand (RANKL).
◦ Denosumab does not bine to bone and its effects on bone turnover diminish within nine months of
treatment completion.
Uses:
◦ Prophylaxis and treatment of osteoporosis→ administered subcutaneously every six months
◦ To reduce skeletal-related events related to metastasis→ higher dose given monthly

Anti-angiogenic drugs target the processes by which new blood vessels are formed and are used in
cancer treatment to restrict tumour vascularisation.
◦ The vascular endothelial growth factor (VEGF) inhibitors bevacizumab and aflibercept
◦ The receptor tyrosine kinase (RTK) inhibitor sunitinib
Anti-angiogenic drugs can be used in combination with the bisphosphonates in the management of
cancer and there is some evidence that this results in a greater MRONJ risk also when used in patients
with a previous history of bisphosphonate use.

Management:

Initial: aim to get the patient as dentally fit as feasible, prioritising preventive care. Higher risk cancer
patients should preferably undergo a thorough dental assessment, with remedial dental treatment
where required, prior to commencement of the drug:
◦ Consider obtaining appropriate radiographs to identify possible areas of infection and pathology;
◦ Undertake any remedial dental work;
◦ Extract any teeth of poor prognosis without delay;
◦ Focus on minimising periodontal/dental infection or disease;
◦ Adjust or replace poorly fitting dentures to minimise future mucosal trauma;
◦ Consider prescribing high fluoride toothpaste.

Give personalised preventive advice to help the patient optimise their oral health, emphasising the
importance of:
◦ Having a healthy diet and reducing sugary snacks and drinks;
◦ Maintaining excellent oral hygiene;
◦ Using fluoride toothpaste and fluoride mouthwash
◦ Stopping smoking;
◦ Limiting alcohol intake;
◦ Regular dental checks;
◦ Reporting any symptoms such as exposed bone, loose teeth, non-healing sores or lesions, pus or
discharge, tingling, numbness or altered sensations, pain or swelling as soon as possible.

Continuing Management:
Low risk patient: If an extraction or another procedure that impacts on bone is required:
◦ Discuss the risks and benefits associated with treatment with the patient to ensure valid consent.
◦ Proceed with the treatment as clinically indicated;
◦ Do not prescribe antibiotic or antiseptic prophylaxis unless required for other clinical reasons;
◦ Advise the patient to contact the practice if they have any concerns, such as unexpected pain, tingling,
numbness, altered sensation or swelling in the extraction area;
◦ Review healing. If the extraction socket is not healed at 8 weeks and you suspect that the patient has
MRONJ, refer to an oral surgery/special care dentistry specialist as per local protocols.
◦ If you suspect a patient has spontaneous MRONJ, refer to an oral surgery/special care dentistry specialist
as per local protocols.
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High risk patient: For medically complex patients for whom you would normally seek advice,
including higher risk patients who are being treated with anti-resorptive or anti-angiogenic drugs for
the management of cancer, consider consulting an oral surgery/special care dentistry specialist with
regards to clinical assessment and treatment planning.
If an extraction is indicated, explore all possible alternatives where teeth could potentially be
retained e.g. retaining roots in absence of infection.

If extraction remains the most appropriate treatment→ same as Low risk

Treatment of MRONJ:
In general, for cases where only a small amount of bone is exposed treatment may include
monitoring, oral hygiene instruction, antibiotics or antibacterial mouth rinses. In cases where a large
amount of bone is exposed, surgery may be indicated. However, the treatment they will receive will
depend on their individual symptoms and clinical presentation.

Dental implants and MRONJ:

Implant placement is not currently contraindicated in patients with osteoporosis. At present, there
is insufficient evidence to indicate whether bisphosphonates have a negative impact on implant
survival in terms of osseointegration.
• Dental implants placed prior to commencement with anti-resorptive or antiangiogenic drugs, of the
small risk of spontaneous MRONJ at those sites and provide information on how to minimise their
risk, for example ensuring excellent oral hygiene at implant site(s).
• Inform osteoporosis patients who consider dental implants during or after treatment with
antiresorptive drugs of the risk of compromised bone healing and MRONJ following the procedure
and the additional small risk of long-term implant failure. Minimise their risk, for example ensuring
excellent oral hygiene at implant site(s).
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Question 33: List reasons for third molar extraction and guidelines for removal an risks of
the procedure?

Assessment before extraction:

1- Reasons for removal; (NICE guidelines) Surgical removal of impacted third molars should be
limited to patients with evidence of pathology, including;
• Symptomatic tooth: Symptoms: pain related to 3rd molar state (exclude other causes) Pericoronitis (NICE):
o Plaque formation is a risk factor but is not in itself an indication for surgery.
o The evidence suggests that a first episode of pericoronitis, unless particularly severe, should not be considered
an indication for surgery.
o Second or subsequent episodes should be considered the appropriate indication for surgery.
• Unrestorable caries
• Non-treatable pulpal and/or periapical pathology
• Cellulitis, abscess and osteomyelitis,
• Internal/external resorption of the tooth or adjacent teeth, fracture of tooth,
• Disease of follicle including cyst/tumour,
• Tooth/teeth impeding surgery or reconstructive jaw surgery, when a tooth is involved in or within the
field of tumour resection.
• Prior to orthognathic surgery

2- Difficulty of removal;
• Patient considerations- MH, PDH. GA/ LA / LA & sedation
• Anxiety
• Journal of Oral and Maxillofac surgery (2010) -60% of patients with asymptomatic disease free 8s
requested extraction. 95% of those with symptoms requested extraction
• Clinical considerations- systemic/ e/o and i/o features (pocketing),
• Radiological considerations-OPT

3- Potential for complications:

Intraoperative:
• Hemorrahge, fractured apices, damage to adjacent tooth or soft tissues, fracture of mandible/
tuberosity.
Postoperative:
• Pain, swelling, bruising, trismus, anesthesia of ID/lingual nerve, infection of bone or soft tissues.

Consider referral to specialist if:

• Operation likely to take >30-40 minutes
• Patient refuses LA Very anxious
• Procedure too complex for LA
• Complicating MH (e.g. osteoradionecrosis risk, osteonecrosis risk,bleeding diatheses)

What is Pericoronitis: inflammation (bacterial infection) of the tissues around the crown of an
incompletely erupted tooth. (acute/ chronic).
Signs and symptoms: Swelling, Soreness, Erythema (operculum), Trismus, Facial swelling, Increased
temp, Regional lymphadenopathy, General malaise.
Causes;
1.Trauma (overerupted upper 8)
2.Food packing and bacterial infection: Plaque accumulation under the flap, which causes
subsequent inflammation and infection. Maybe impossible for the patient to reach and clean
adequately.
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May be associated with;
1.poor OH (unavoidable in some cases)
2.Stress
Treatment:
• Irrigate with saline/ CHX under operculum
• Home use of MW
• Antibiotics if systemic features of infection or pt. at significant risk (metronidazole 400 mg tds week
or Amoxicilin 500 mg tds for a week)
• Pain relief: analgesics NSAIDS (Ibuprofen)
• If severe → hospital referral
• Consideration of status of tooth when infection settled (extraction may be indicated).
Contraindications to removal:
• Impacted/unerupted & expected to be functional
• No history or evidence of pertinent local or systemic pathology
• MH – complications of removal > complications of leaving
• Increased risk of complications (IDN, mandibular fracture)

NB; Not crowding or prophylaxis (no evidence for removal of contralateral/ ipsilateral if disease-free)

Assessing level of difficulty:

1- Patient considerations: Patient attitude and co-operation, Phobias (re; management), Previous
experience Informed consent.
2- Clinical assessment in general: mouth opening, size/ spread of the tongue, mandibular retrosion
3- Clinical assessment Local: tooth position, state of eruption, caries or perio. Infection, adjacent
structures, relation to 2nd molar
4- Radiological assessment: (OPT→ type of impaction: mesial angle, distal angle, horizontal, vertical
or oblique), path of eruption, relation to antrum, tuberosity, IDN, ramus)
5- Obstucules to removal:
• Extrinsic→depth of bone, adjacent teeth
• Intrinsic→ curvature of roots, caries, infection

Winter classification:
White line - along occlusal surface shows axial inclination (eg m'ang)
Amber line - from bone distal to 8 to top of mesial interseptal bone; shows degree of eruption
Red line - dropped from amber line to point of elevator application shows depth of impaction
increase of 1mm = 3x difficulty
>5mm = GA (some suggested)

Winter’s lines, height of mandible, angle of second molar, root shape and deviation, follicle, exit path.
 113
Question 34: Define infective endocarditis and mention the guidelines for antibiotics
prophylaxis?

Infective endocarditis (IE) is defined as an infection of the endocardial surface of the heart, which
may include one or more heart valves, the mural endocardium, or a septal defect.
•Its intracardiac effects include severe valvular insufficiency, which may lead to intractable congestive
heart failure and myocardial abscesses. If left untreated, IE is almost inevitably fatal.

The incidence of IE is approximately 1.7-6.2 cases per 100,000 patient years.

• Infective endocarditis is a rare condition with significant morbidity and mortality. It may arise after bacteraemia in a
person with a predisposing cardiac lesion.
Symptoms:
• High T (>38), chills, night sweats, shortness of breath, cough, heart murmur, fatigue, muscle and joint pain.
• Spotty red rash on the skin (petechiae)
• Narrow redesh-brown lines of blood that run underneath the nails,
• Painful raised lumps that develop on fingers and nails
• Painful red spots that develop on palms of the hand and soles of the feet
• Mental confusion

In 2008 NICE:
The guideline recommended that people at risk of infective endocarditis having interventional
procedures (dental procedures, upper and lower respiratory tract procedures, upper and lower
gastrointestinal tract procedures, genitourinary tract procedures) should not be offered antibiotic
prophylaxis against infective endocarditis.

IN 2015 NICE guidelines update: (adding the word routinely)

Antibiotic prophylaxis against infective endocarditis is not recommended routinely:
•For people undergoing dental procedures
•For people undergoing non-dental procedures at the following sites:
1.upper and lower gastrointestinal tract
2.genitourinary tract; this includes urological, gynaecologicaland obstetric procedures, and
childbirth
(upper and lower respiratory tract; this includes ear, nose and throat procedures and bronchoscopy.)
Chlorhexidine mouthwash should not be offered as prophylaxis against infective endocarditis to
people at risk of infective endocarditis undergoing dental procedures.

Routinely' has been added to the recommendation of prophylaxis for consistency with the
recommendation of patient advice:
Doctors and dentists should offer the most appropriate treatment options, in consultation with
the patient and/or their guardian. In doing so, they should take account of the
recommendations in this guideline and the values and preferences of patients, and apply their
clinical judgment.

Patient advice:
Healthcare professionals should offer people at increased risk of infective endocarditis clear
and consistent information about prevention, including:
• The benefits and risks of antibiotic prophylaxis, and an explanation of why antibiotic prophylaxis is no longer routinely
recommended
• The importance of maintaining good oral health, eradication of chronic bacterial infections
• Symptoms that may indicate infective endocarditis and when to seek expert advice
• The risks of undergoing invasive procedures, including non-medical procedures such as body piercing or tattooing.
• Disinfection of wounds, strict infection control
• Limit the use of infusion catheters
• No self medication with antibiotics.
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Healthcare professionals should regard people with the following cardiac conditions as
being at increased risk of developing infective endocarditis:
1- Acquired valvular heart disease with stenosis or regurgitation
2- Hypertrophic cardiomyopathy
3- Previous infective endocarditis
4- Structural congenital heart disease, including surgically corrected or palliated structural conditions, but excluding isolated
atrial septal defect, fully repaired ventricular septal defect or fully repaired patent ductus arteriosus, and closure devices that
are judged to be endothelialised
5- Valve replacement.

Rationale for not prescribing prophylaxis:

The restriction of indications for antibiotic prophylaxis was initiated in 2002 because of
changes in pathophysiological conceptions and risk–benefit analyses as follows:
• Low-grade but repeated bacteraemia occurs more frequently during daily routine activities such as tooth
brushing, flossing or chewing, and even more frequently in patients with poor dental health.
• The accountability of low-grade bacteraemia was demonstrated in an animal model. The risk of IE may
therefore be related more to cumulative low-grade bacteraemia during daily life rather than sporadic
high-grade bacteraemia after dental procedures.

• Widespread use of antibiotics may result in the emergence of resistant microorganisms.

• The efficacy of antibiotic prophylaxis on bacteraemia and the occurrence of IE has only been proven in
animal models. The effect on bacteraemia in humans is controversial.
• No prospective randomized controlled trial has investigated the efficacy of antibiotic prophylaxis on the
occurrence of IE and it is unlikely that such a trial will be conducted given the number of subjects
needed.
• The estimated risk of IE following dental procedures is very low. Antibiotic prophylaxis may
therefore avoid only a small number of IE cases, as shown by estimations of 1 case of IE per 150 000
dental procedures with antibiotics and 1 per 46 000 for procedures unprotected by antibiotics.

In the 2015 ESC Guidelines for the management of infective endocarditis (European society of
cardiology):
The present guidelines maintain the principle of antibiotic prophylaxis in high-risk patients:
(1) Patients with a prosthetic valve or with prosthetic material used for cardiac valve repair: these
patients have a higher risk of IE, a higher mortality from IE and more often develop complications of the
disease than patients with native valves and an identical pathogen. This also applies to transcatheter-
implanted pros-theses and homografts.
(2) Patients with previous IE: they also have a greater risk of new IE, higher mortality and higher
incidence of complications than patients with a first episode of IE.
(3) Patients with untreated cyanotic congenital heart disease (CHD) and those with CHD who have
postoperative palliative shunts, conduits or other prostheses. After surgical repair with no residual
defects, the Task Force recommends prophylaxis for the first 6 months after the procedure until
endothelialisation of the prosthetic material has occurred.

Dental procedures at risk:

At-risk procedures involve manipulation of the gingival or periapical region of the teeth or
perforation of the oral mucosa (including scaling and root canal procedures).
• The use of dental implants raises concerns with regard to potential risk due to foreign material at the
interface between the buccal cavity and blood.
• Very few data are available. The opinion of the Task Force is that there is no evidence to
contraindicate implants in all patients at risk.
• The indication should be discussed on a case-by-case basis. The patient should be informed of the
uncertainties and the need for close follow-up.
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Antibiotics: target oral streptococci: (30 to 35% of IE cases associated with these species):