Anatomy:-

1. Bones that make up the zygomatic arch:-

• Temporal bone.
• Zygomatic bone.
2. What artery passes over it?
Transverse facial artery
3. What are the clinical signs of fractured zygoma or zygomatic arch?
• Flattening of the zygomatic prominence. Depression in the
zygomatic arch (flattening of cheekbone).
• Lowered lateral portion of palpebral fissure.
• Limited eye movement due to tethering of the extra-ocular
muscles.
• Mechanical interference with the coronoid process (Limited
mandibular movement).
• Unilateral epistaxis.
• Subconjunctival haemorrhage
• Circumorbital ecchymosis.
• Numbness in the inferior orbital nerve innervated area and cheek.
• Diplopia.
• Pain and swelling.
4. Foramina of base of skull:-
a. Foramen rotundum, sphenoid  maxillary division of trigeminal nerve.
b. Internal acoustic meatus, petrous part of temporal  CN VII, VIII,
labyrinthine artery.
c. Jugular foramen, petrous part of temporal + occipital  CN XI, X, XI
(spinal), inferior petrosal sinus, sigmoid sinus, posterior meningeal artery.
d. Hypoglossal canal  occipital.
e. Foramen magnum  medulla oblongata, vertebral arteries, spinal of
spinal accessory nerve.
f. Incisive foramen  palatine process of maxilla  nasopalatine nerve,
sphenopalatine artery.
g. Greater palatine foramen  palatine bone (horizontal plate)  Greater
palatine nerves and vessels.
 h. Lesser palatine foramen  palatine bone (pyramidal process)  lesser
palatine nerves and vessels.
i. Foramen ovale  sphenoid  mandibular division of trigeminal nerve,
accessory meningeal artery, lesser petrosal nerve, emissary vein.
j. Foramen spinosum  sphenoid  middle meningeal vessel + meningeal
branch of mandibular division.
k. Carotid canal  temporal  ICA, ICN plexus (sympathetic).
l. Petrotympanic fissure  temporal  chorda tympani.
m. Stylomastoid foramen  temporal  facial nerve + stylomastoid artery.
n. Optic canal  sphenoid  optic nerve + ophthalmic artery.
o. Superior orbital fissure  between greater and lesser wings of the
sphenoid 
• Branches of ophthalmic (nasocilliary, lacrimal, frontal)
• CN III.
• CN IV.
• CN VI.
• Superior and inferior ophthalmic veins.
p. Inferior orbital fissure  between (the greater wing of sphenoid) and the
(orbital process of maxilla and palatine bones).
• Maxillary nerve.
• Zygomatic nerve.
• Infraorbital vessels.
5. Neuroanatomy:
• Parasympathetic  CN III, VII, IX, X
• Sympathetic  superior sympathetic cervical ganglion.
I. Eye:
• Parasympathetic:

Edinger-Westphal CN III  oculomotor root of ciliary ganglion Ciliary ganglion

Sphincter pupillae (constriction of pupil)

Short ciliary
Ciliary muscle (change shape of lens during
accommodation)

II. Lacrimal gland:

Superior CN VII  Greater petrosal nerve Pterygopalatine ganglion
salivatory nucleus

Lacrimal gland

III. Submandibular and sublingual glands

Same as lacrimal gland but instead of greater petrosal nerve it’s chorda
tympani exiting through the petrotympanic fissure and synapse in the
submandibular ganglion.
IV. Parotid gland:
Inferior salivatory CN IX  Tympanic branch  lesser petrosal Otic ganglion
nucleus  foramen ovale  infratemporal fossa

Parotid gland
Auriculotemporal
Oral Medicine:-

1. What diseases cause desquamative gingivitis?

• Pemphigus vulgaris.
• Mucous membrane pemphigoid.
• Lichen planus
2. What is the treatment of it?
• Improving oral hygiene.
• Minimizing irritation of the lesions.
• Specific therapies for the underlying disease where available.
• Local or systemic immunosuppressive or corticosteroid therapy.
3. Median rhomboid glossitis, describe the lesion, what are the causes, what
other lesions do you suspect to see? How would you biopsy the lesion?
• Causes:-
a. Smoking.
b. Denture wearing.
c. Corticosteroid inhalers.
d. HIV infection.
4. Lump in the palate, what is your differential diagnosis?
• Dental abscess.
 • Neoplasm (salivary gland, Kaposi’s sarcoma)
• Papilloma.
• Torus palatinus.
• Unerupted teeth.
5. What are the causes of xerostomia? Clinical features?

Causes:-

• Drugs: Atropine, Antidepressents, antihypertensives, phenothiazenes,

antihistamines, antireflux agents, opioids, cytotoxic drugs, retinoids,
diuretics, ephedrine.
• Radiotherapy.
• Graft-versus host disease.
• Sjogren’s syndrome.
• Dehydration.
• Psychogenic.

Clinical features:-

• Difficulty in swallowing.
• Difficulty controlling dentures.
• Difficulty in peaking.
• Mouth soreness.
• Unpleasant taste.
• Lips adhere to one another.
• Dental mirror sticks to the mucosa.
• Lipstick or food debris sticking to teeth.
• Lack of usual poling of saliva in the floor of the mouth.
• Saliva not expressible from parotid duct.
• Lobulated tongue, usually red, with partial or complete depapillation.
• Complications of xerostomia:-
a. Dental caries.
b. Candidiasis, which causes:-
I. Burning sensation.
II. Taste changes.
III. Intolerance to acids and spices.
 IV. Mucosal erythema.
V. Angular stomatitis.
c. Ascending suppurative sialadenitis.
6. What is the process of dental caries?
• Dental bacterial plaque metabolizes refined carbohydrates (mainly
sucrose) to organic acids, which decalcify enamel.
7. What are the clinical features of HSV primary infection?
• Fever.
• Headaches.
• Malaise.
• Cervical lymphadenopathy.
• Fluid filled vesicles in the gingiva and other areas (lips, tongue, buccal and
palatal mucosa).
• Vesicles rupture in a few hours to form painful ulcers with red inflamed
margins.
• The clinical episode runs for 14 days then ulcers heal without scarring.
8. What is the treatment of HSV primary infection?
• Bed rest.
• Soft diet.
• Hydration.
• Paracetamol.
• Chlorhexidine.
• In severe cases of HSV infection acyclovir 200 mg 1X5X5 suspension,
under 2 years 100 mg 1X5X5.
9. What is epulis fissuratum?
• It is a painless, firm swelling with smooth pink surface usually in the buccal
sulcus related to complete denture, especially anteriorly. Pressure from a
denture flange causes chronic irritation and hyperplastic response.
Diagnosis is clinical but excisional biopsy may be indicated. The denture
flange should be relieved to prevent recurrence.

10.What are Fordyce spots? What is the prevalence of Fordyce spots?

• They are sebaceous glands containing neutral lipids similar to those foud
in skin sebaceous glands, but they are not associated with hair follicle,
prevalence is 80% of the population.
Infections control:-

1. What are the types of gloves?

• Examination gloves: Single use, non-sterile.
• Surgical gloves: Single use, sterile.
• Non-medical gloves: Sanitize after use.
2. What is the difference between vacuum and non-vacuum autoclaves?
• Type N (Non-vacuum): relies on gravity for air displacement, for
unwrapped instruments, maximum storage is 21 days.
• Type B and S (Vacuum): relies on a mechanism that creates vacuum, for
wrapped instruments and packages, maximum storage is 60 days.
3. What are the cycles of auto-clave?
• 121-124 C for 15 minutes at 104 kPa.
• 134-137 C for 3 minutes at 207 kPa.

Orthodontics:-

1. What cephalometric changes would you expect if you use medium opening
activator???
• Increase in MMPA because of reduction of deep bite and super
eruption of molars, this appliance is used for treating deep bite.
2. Wat are the causes of diastema? What are the types of mesiodens?
Functional appliances? What do they consist of? What action do they
perform?
• Diastema:-
a. Midline supernumerary tooth.
b. Missing or small lateral incisors.
c. Incisor proclination in class II div. 1.
d. Tooth/arch size discrepancy.
e. High frenal attachment.
3. What is Frankel appliance? What are the types of it?
4. What are types of supernumerary teeth?
• Conical.
• Tuberculate.
• Supplemental teeth.
5. What are the dental effects of finger and thumb sucking?
 • Proclination of upper incisors.
• Retroclintion of lower incisors.
• Increase in the overjet.
• Reduce the overbite.
• Crossbite tendency of the buccal segment.
6. Draw a design of removable orthodontic appliance for posterior cross bite?
7. What are the factors that govern the treatment of anterior cross bite?
• Type of movement required (bodily or simple tipping) this I
determined by assessing the angulation of the teeth involved in the
cross bite.
• The amount of overbite expected at the end of treatment.
• The presence of space to accommodate the teeth to be removed.
• Is reciprocal movement of opposing teeth required?
8. What factors govern the treatment of posterior cross bite?
• Number of teeth displaced.
• Whether this displacement is skeletal or dental in nature?
• Inclination of teeth involved.
• Upper arch expansion is considered more stable if teeth were palatally
tilted.

Prosthodontics:-

1. Patient has a lower complete denture, asking about muscles affecting the
areas.
2. Kennedy classification and design.
• Support.
• Major connector.
• Minor connector.
• Retention.
•
3. RPI system advantages?
• Mesial rest, proximal plate and I-bar: Changing the fulcrum of
rotation of the RPD which results in the reduction of stress on the
abutment tooth acting as a stress breaker. The whole system allows
minimizing of horizontal and leverage forces on the tooth and
 directing forces along the vertical access of the tooth during
tissuewards movement in distal extension dentures.
4. What are the functions of guiding planes?
• Provide for one path of placement.
• Provide retention and stability against horizontal rotation of the
denture.
• Eliminate food traps between abutment teeth and RPD.
5. What factors govern support in RPD?
• Quality of residual ridge.
• The extent to which the residual ridge is covered by the denture
base.
• The accuracy and type of impression registration
• The accuracy of denture bases
• The design characteristics of the component parts of the partial
denture framework.
• Occlusal load.

Radiology:-

1. How do we take standard occlusal x-ray?

• Patient is seated with head supported and occlusal plane horizontal
and parallel to the floor and is asked to support a thyroid shield.
• The image receptor (preferably wrapped) is placed centrally with
its long axis crossways (AP in children) in the patient’s mouth and
the patient is asked to bite gently.
• X-ray tubehead is positioned above the midline of the patient
aiming downwards through the bridge of the nose at an angle 65-
70 to the image receptor.
2. What are the uses of bitewings?
• Detection of dental caries.
• Monitoring progression of dental caries.
• Assessment of existing restorations.
• Assessment of periodontal status.

Cranial nerve examination of CN III, IV, V, VI, VII:-

 • Explain to the patient what you want to do.
• CN III (Oculomotor)+ CN IV and VI: Cover one eye and follow the pen
upwards, downwards, medially, superio-medially in an H shape, then
switch to the other eye and repeat. Use light to test for accommodation.
• CN V:
a. Touch with a cotton swab (beware not to examine too laterally in the
mandible because of C2 and C3)
b. Corneal reflex.
c. Muscles of mastication (ask to clench the jaws while palpating the
muscles of mastication).
d. Ask the patient to perform a wide range of mandibular movements
including maximum opening and lateral excrusive movements.
e. Jaw jerk reflex
• CN VII:
a. Inspect for asymmetry and involuntary movements.
b. Ask the patient to:-
1. Raise both eyebrows.
2. Frown.
3. Close both eyes tightly.
4. Smile.
5. Puff out both cheeks.
6. Pout.
c. Taste sensation.

Trauma:-

Splinting time:-

1. Avulsion  2 weeks functional splint.

2. Luxation - 2-4 weeks functional splint.
3. Apical and middle third #  4 week functional splint.
4. Coronal third #  8 weeks functional splint.
5. Dento-alveolar #  3-4 weeks of rigid splint.
6. Intrusion open apex >7mm  8 weeks functional splint.

Intrusion:-
Px depend on the extent of injury and the root formation

Open apex:-

• <7 mm may erupt, wait 2-4 week, if no movement  ortho

• >7mm  disimpaction + surgical repositioning, Functional splint  4-8
weeks

Close apex:-

• <7mm  ortho.
• >7mm  surgical repositioning, functional splint  4-8 weeks.

In intrusive injury, pulp necrosis is:-

• 60% in open apex.

• 100% in closed apex.

In extrusive and lateral luxation:-

• 5% in open apex

In lateral luxation:-

• 75% in closed apex compared to 55% for extrusive luxation.

Factors that determine Px of avulsion:-

1. EADT.
2. EAT < or > 30-45?
3. Storage medium.
4. Root maturity.

Necrosis can be diagnosed within 3 months of the injury but may not be evident
until 2 years.

Factors to decide whether necrosis occurred:-

1. Sensitivity testing.
2. Tooth dicolourtion
3. TTP
4. PA inflammation
 5. Arrest of root development

MIH:-

Aetiology unknown, possible factors:-

1. Asthma.
2. Pneumonia.
3. URTI
4. Otitis media.
5. Tonsillitis.
6. Antibiotics.
7. Digoxin in mother’s milk.
8. Problems in pregnancy.
9. Chickenpox.

Problems with MIH:-

1. Porous enamel  Sensitivity.

2. Hypomineralization  Weak enamel (prone to break down).
3. Discolouration.
4. Difficult to anesthetize.
5. Difficult to restore especially with composite.

Management:-

Stage 1  Identify affected teeth.

Stage 2  resolve sensitivity and remineralization.

Stage 3  prevention of caries.

Stage 4  Assess px of 1st molars whether to extract or restore.

Stage 5  maintenance.

a. Sensitivity:-
1. Treat sensitivity with CPP-APP.
2. 0.4% Stannous fluoride gel daily.
3. 5% NaF varnish (Duraphat).
4. Sensitivity tooth pastes.
 b. Fissure sealant.
c. Restoration. (Amalgam, composite, GIC).
d. Long term prognosis (if poor  exo at the right time)

Delayed eruption of teeth:-

1. Generalized
a. Hereditary gingival fibromatosis.
b. Cleidocranial dysostosis.
c. Hypothyroidism.
d. Hypopituritism.
e. Nutritional deficiency.
f. Down’s syndrome.
g. Turner’s syndrome.
2. Localized
a. Supernumerary tooth.
b. Crowding.
c. Ectopic position of the tooth germ.

Infection:-

Infection control policy:-

1. Minimize risk of bood-borne infection transmission (sharps injury)

2. Patient evaluation
3. Personal protection
4. Decontamination of instruments.
5. Disinfection and sterilization.
6. Management of clinical waste.
7. Hand hygiene.
8. Decontamination of reusable instrument.
9. The use of PPE.
10.Spillage procedure.

Examples of single use instruments:-

1. Saliva ejectors.
2. Aspirator tips.
3. Matrix bands.
 4. Three-in-one syringe.

Hand hygiene should be practised at the following key stages in the

decontamination process so as to minimise the risk of contamination:

• before and after each treatment session;

• before and after the removal of PPE;

• following the washing of dental instruments;

• before contact with instruments that have been steam-sterilized

(whether or not these instruments are wrapped);

• after cleaning or maintaining decontamination devices used on dental

instruments;

• at the completion of decontamination work. For floor and general surface

cleaning, the national colour coding scheme for cleaning materials and
equipment in primary care medical and dental premises may be useful:

• red – for wash-rooms;

• blue – for offices;

• green– for kitchens;

• yellow – for clinical and decontamination areas.

Areas and items of equipment local to the dental

chair that need to be cleaned between each patient

include:

• local work surfaces;

• dental chairs;

• curing lamps;

• inspection lights and handles;

• hand controls including replacement of covers;

• trolleys/delivery units;

• spittoons;

• aspirators;

• X-ray units

the TVC should

be expected to lie in the range 100 to 200 colony

forming units per millilitre (cfu/ml). TVC = Total viable count

DUWLs should be flushed for at least two minutes at the beginning and end of
the day and after any significant period when they have not been used (for
example, after lunch breaks). In addition, they should also be flushed for at least
20–30 seconds between patients.

Mode of infection transmission in dental practice: -

1. Direct or indirect contact:

a. Viruses: HSV, VZV, EBV.
b. Bacteria: MRSA
2. Via blood stream:
a. HBV.
b. HIV.
c. HCV.
3. Airborne or respiratory infection:
a. Bacteria: TB
b. Viruses: Influenza.

Caries risk determination: -

1. Social history:
a. Social deprivation.
b. Caries in siblings.
c. Socio-economic status.
d. Dental knowledge.
e. Dental attendance.
2. Medical history:
 a. Any physical disability.
b. Any medications that would cause xerostomia.
c. Any medications that contain sugars.
3. Plaque control: oral hygiene practices including daily brushing and
interdental cleaning.
4. Dietary habits: frequency of daily sugar intake, amount.
5. Fluoride: fluoride tooth paste? Lived in a fluoridated area.
6. Saliva: frothy or clear? Thick or thin?
7. Clinical evidence:
a. New caries
b. Previous caries
c. Heavily restored dentition.
d. Smooth surface caries.
e. Missing teeth due to caries.
f. Orthodontic appliance.

Radiology: -

Indications of BW: -

1. Caries detection.
2. Caries progression monitoring.
3. Assessment of existing restorations.
4. Assessment of the periodontal status.

Too dark film:

1. Overexposure:
a. Exposure time.
b. Faulty x-ray equipment.
2. Overdevelopment:
a. Too hot.
b. Development time.
c. Too concentrated
3. Fogging:
a. Poor storage.
b. Old film.
c. Faulty cassette, allowing ingress of light.
 d. Faulty darkroom and or safe-light.
4. Thin patient.

Too pale film:

1. Underexposure:
a. Exposure time.
b. Faulty x-ray equipment.
2. Underdevelopment:
a. Too cold.
b. Development time was short.
c. Too diluted. developer
d. Exhausted developer.
e. Developer contaminated by fixer.
3. Film packet back to front (film marks)
4. Thick patient’s tissue.

Low contrast:

1. Fogging (same above)

2. Processing error 
a. Underdevelopment.
b. Overdevelopment.
c. Developer contaminated by fixer.
d. Inadequate fixation time.
e. Fixer solution exhausted.

Image blurred:

1. Movement of the patient during exposure.

2. Excessive bending of the film packet.
3. Overexposure.
4. Poor positioning in OPG

Radiographic assessment of caries activity:

1. High risk  every 6 months.

2. Moderate risk  every 12 months.
3. Low risk:
 a. Adults: 2 years.
b. Children: 12-18 months.

Orthodontics:

Anterior cross-bite, what to check for?

1. Normal skeletal pattern (check for anterior displacement of the mandible

and whether patient can achieve edge-to-edge).
2. Adequate space in the arch  primary canines may need to be extracted.
3. Adequate overbite  for a stable result.

General design is:

• Z-spring or screw.
• Adams clasp on 6s or and Es.
• Fitted labial arch anteriorly (southend clasp).
• Posterior capping.

Posterior cross-bite:

Midline screw turned by the patient once or twice a week and double Adams
clasp on upper 6s and Es.

Myfounctional appliances  dentoalveolar and skeletal changes.

Effects of thumb sucking:

1. Asymmetric anterior open bite.

2. Increased overjet with proclined upper incisors and retroclined lower
incisors.
3. Class II buccal segment relationship.
4. Unilateral posterior cross-bite with displacement.

Success of primary canine extraction:-

1. Early detection <12 years.

2. Adequate space for 3s to erupt.
3. Mild/moderate canine displacements.

Types of supernumerary teeth:

 1. Conical.
2. Tuberculate.
3. Supplemental.
4. Odontomes.

Dental and oral features of CLP:

1. Delayed dental development (especially on the cleft side).

2. Impacted first permanent molars (shortened dental arch).
3. Hypodontia (upper 2s in 50%).
4. Microdontia and hypoplasia particularly upper 1s.
5. Supernumerary.
6. Impacted cleft canine.
7. Rotated tooth positions.

Prevention:

What are the actions of fluoride?

• Systemic:
a. Improves crystallite structure, crystal size and reduced acid
solubility. (flouroapatite crystals).
b. Rounded cusps, shallow fissures.
• Local:
a. Enhanced remineralization.
b. Inhibits demineralization.
c. Inhibits plaque formation.
d. Inhibits transformation of sugars into acids by acidogenic bacteria.
e. Increased fluoride concentration inhibits the formation of extra-
cellular polysaccharides.

STD  Maximum dose in which bellow systemic effects are unlikely. 1 mg/kg

PLD  minimum dose associated with fatality. 5 mg/kg

CLD  dose in which survival is unlikely  32-64 mg/kg

PPM = 1 mg/L
1000 PPM = 1 mg/ml

<5 mg/kg  milk

>5 mg/kg  refer to hospital for gastric lavage, calcium gluconate + emetic.

Delayed eruption causes:

General:

1. Malnutrition.
2. Rickets.
3. Hypothyroidism.
4. Down’s syndrome.
5. Gardner’s syndrome.
6. Cleidocranial dysostosis.
7. Hereditary gingival fibromatosis.

Local:

1. Presence of supernumerary teeth.

2. Trauma.
3. Dentigerous cyst.
4. Dilaceration.
5. Abnormal position of crypt.
6. Retention of primary tooth.
7. Crowding.

Types of supernumerary teeth:

By shape:

1. Conical.
2. Tuberculate.
3. Supplemental tooth.
4. Odontoma.

By position:

1. Distomolar.
2. Paramolar.
 3. Mesiodens.

Effects on dentition:

1. No effect.
2. Crowding.
3. Displacement.
4. Failure of eruption.

Complications of injuries to primary teeth:

1. Discoloration.
2. Loss of vitality.
3. Ankyloses.
4. Injuries to the permanent teeth: dilaceration, hypoplasia, arrest of
development.

E+D+P#

Factors:

1. Size of exposure site.

2. State of root development.
3. Time since the injury.

Pulp capping <1mm, <24 hours for complete and incomplete roots.

Partial pulpotomy >1mm, >24 hours for both.

Complete pulpotomy  large contaminated exposures for longer times.

Success rate for complete pulpotomy  72%

For partial pulpotomy  96%

Root fractures

Apical 1/3

Middle 1/3  rigid splinting for hard-tissue union for 12 weeks. Recent evidence
suggests flexible splinting for 4 weeks.
Apical 1/3  flexible splint for 4 months.

If extends coronally to oral environment  extract coronal fragment.

If # extends below the alveolar crest  crown lengthening or orthodontic

extrusion.

Avulsion

Factors:

1. Time from loss to re-implantation. 60 minutes is the critical time.

2. Extra-alveolar dry time.
3. State of root development.
4. Storage medium. Saline > milk > water > air.
5. Splinting time 7-10 days, prolonged splinting promotes ankyloses.

Sequelae of avulsion:

1. Ankyloses.
2. Inflammatory resorption.
3. Pulp death.

Implants:

• For emergence profile, the implant should be placed 2-3 mm below

the gingival margin.
• Healing abutment for 3-4 weeks for soft tissue healing.
• Chin and ramus (external oblique ridge) are common sites for
harvesting bone.
• 3 months between bone grafting and implant placement, if left too
long there’s a risk that the graft will be resorbed.

Types of veneer preparation:

1. Window preparation  incisal edge maintained.

2. Featherhead preparation  ends at the incisal edge.
3. Bevel preparation  incisal edge reduced with no preparation of palatal
surface.
4. Incisal overlap preparation  palatal preparation included.
Median diastema:

Prevalence  98% at 6 years, 49 % at 11 years, 12-18  7%

Causes:

1. Prominent labial frenum.

2. Proclination.
3. Physiological.
4. Presence of a supernumerary tooth.
5. Missing upper lateral incisors.
6. Peg shaped upper lateral incisors.
7. Large jaw and small teeth.

What would you see if you suspect a labial frenum?

1. Blanching of incisive papilla when stretching the labial frenum.

2. P.A x-ray  V-shaped notch in the interdental bone.
3. Anterior teeth may be crowded

Management:

• Before the eruption of upper 3s:

1. If <3mm and canines are unerupted, observe and monitor after
eruption of canines.
2. If >3mm and canines are unerupted may need to approximate the
central incisors, care will be required not to resorb roots of upper 2s
against crowns of upper 3s.
• After the eruption of upper 3s:
1. Accept.
2. Orthodontics.
3. Composite.

Palatally displaced canines:

Prevalence  2%, F>M, bilateral in 17-25%

Cephalometric changes in twin block treatment:

Skeletal:
 1. Increase in SNB due to mandibular growth.
2. Reduction in ANB due to overjet reduction.
3. Increase MMPA due to increase in LFH.

Dental:

1. Reduction in Upper 1 to maxillary plane angle due to retroclination of

upper incisors.
2. Increase in lower 1 to mandibular plane angle due to proclination of lower
incisors.

Skeletal changes:

1. Restraint of forward maxillary growth.

2. Optimization of mandibular growth.
3. Forward movement of glenoid fossa.
4. Increase of LFH.

Dental changes:

1. Palatal tipping of upper incisors.

2. Labial tipping of lower incisors.
3. Inhibition of forward movement of maxillary molars.
4. Mesial and vertical eruption of mandibular molars.

Causes of CLP:

1. Environmental.
2. Genetic.
3. Maternal smoking, alcohol, and phenytoin.

Dental anomalies:

1. Increased prevalence of hypodontia.

2. Supernumerary teeth.
3. Teeth adjacent to the cleft are displaced.
4. Delayed eruption.
5. Increased incidence of hypoplasia.
6. Posterior crossbite.
7. Anterior openbite.
Steps of RPD:

1. Outline saddle.
2. Plan support (occlusal rests).
3. Plan direct retention.
4. Plan indirect retention.
5. Assess bracing required. (provided by):
a. Connector.
b. Maximum saddle extension.
c. Reciprocal arms of clasps.
6. Connect the denture.
7. Reassess (as simple as possible and aesthetics).
8. Instructions to the technician.

RPI system: providing support, retention and minimum stress on the distal
abutment tooth.

1. Mesial rest  on the last tooth. This position, in relation to the I-bar
provides a modest degree of indirect retention.
2. Minor connector between the rest and the lingual bar engages the mesial
surface of the abutment tooth and helps resist distal movement of the
denture framework.
3. Proximal plate  abuts a guide plane on the distal surface of the
abutment tooth to give the denture a single path of insertion and
contributes to reciprocation of the clasp along with the minor connector
and mesial rest.
4. I-bar  direct retention. Being distal to the mesial rest, displacement of
the saddle during function results in the clasp being disengaged in a
gingival direction. Reducing stress on the tooth.

Altered case technique  to record the distal extension saddle under load to
improve the support of the denture, thereby reducing the rotation of the
denture around the distal rest.

Balanced occlusion: Simultaneous contact between upper and lower teeth on

both sides in intercuspal position.
Balanced articulation: Simultaneous contact between upper and lower teeth on
both sides in lateral and protrusive movements.

Aim of balanced occlusion in complete dentures:

• Occlusal forces are transmitted evenly to the alveolar ridges,

reducing the risk soreness of the alveolar mucosa.
• Retention reinforced to avoid have deflective contact.

Causes of angular cheilitis:

1. Ill-fitting dentures.
2. Chronic atrophic candidosis (denture induced stomatitis).
3. Xerostomia.
4. Deficiency of Fe, Folate, vitamin B12 or riboflavin.
5. Immune deficiency, DM or HIV.

Investigations:

1. Salivary flow rate (Investigate for underlying xerostomia)

2. Investigate for immune deficiency.
3. CBC.
4. Crohn’s disease.

Rx:

1. Instruct patients to leave dentures out at night.

2. Antifungals (miconazole and fluconazole).
3. Check dentures.

Erythema multiforme:

Clinical features:

• Blood stained ulcerations and crusting in the lips.

• Conjunctivae and skin may also be affected.
• In Stevens-Johnson’s syndrome, you expect to find fever, ocular,
genital, nasal and urethral lesions.

Causes:
Autoimmune condition related to HSV, HCV, mycoplasma and drugs such as
sulphonamides, cephalosporins and barbiturates.

Complications of xerostomia:

1. Dental caries.
2. Candidal infection.
3. Bacterial sialadenitis  penicillinase resistant antibiotic (Flucloxacillin).
4. Disturbed taste sensation.
5. Difficulties in denture retention.

Causes of xerostomia:

1. Medications:
a. Antihypertensive.
b. TCA.
c. Atropine, anticholinergic drugs.
d. SSRI.
e. Antipsychotics.
f. Antihistamines.
g. Phenothiazines.
h. Cytotoxic drugs.
i. Retinoids.
2. Radiotherapy.
3. Stress and anxiety.
4. Dehydration.
5. Uncontrolled D.M.
6. Sjogren’s syndrome.
7. Smoking.
8. Mouth breathing.
9. Graft-versus-host disease.
10.Sarcoidosis.
11.HIV.

Salivary substitutes:

1. Carboxymethycellulose (Glandosane).
2. Saliva Orthana (fluoride).
Salivary stones treatment:

1. Surgical removal of the stone with stay suture.

2. Surgical removal of the stone along with the gland.
3. Lithotripsy (US).

Bilateral parotid swelling:

1. Sialosis.
2. Mumps.
3. Sjogren’s.
4. HIV/AIDS.
5. Sarcoidosis.
6. Warthin’s tumour.

Sialosis  liver disease, malnutrition, D.M.

Ney surveyor:

1. Platform on which the base is moved.

2. Vertical arm that supports the superstructure.
3. Horizontal arm from which surveying tool suspends.
4. Table on which the cast is attached.
5. Base on which the table swivels.
6. Paralleling tool or guideline marker.
7. Mandrel for holding special tools:
a. Undercut gauge.
b. Carbon marker.
c. Wax trimmer.
d. Surveying blade.

Purpose of surveyor:

1. Establish path of insertion.

2. Locate and measure undercuts used for retention.
3. Locate undesired undercuts for block-out.
4. To determine whether there are areas either in teeth or bone that needs
to be eliminated surgically.
 5. Planning the proximal tooth surfaces preparation to be made to provide
guiding planes.
6. Define the height of contour on abutment teeth.
7. Record cast position in relation to the path of insertion for future
references. This may be done by locating three dots or parallel lines on
the cast.

Gold wrought wire  0.75 mm

SS wrought wire  0.5 mm

Cast Cr-Co 0.25 mm

Possible solutions for free-end saddle:

1. Maximize indirect retention by using mesial rests and clasps on mesial

aspects of the abutment tooth and using lingual plate design.
2. Muco-compressive impression technique of saddle area to reduce
displacement tissue wards during function.
3. Use fewer and smaller teeth.
4. Maximize base extension.
5. RPI system.
6. Stress breaker.

Optimize retention and stability in CD:

1. Maximum extension of denture base.

2. Peripheral seal.
3. Close adaptation of denture base to mucosa.
4. Placement of teeth in neutral zone.
5. Correct shape of the polished surfaces so that muscle action tends to re-
seat the denture.
6. Post-dam to ensure peripheral seal.
7. Balanced occlusion free from interfering contacts.

Causes of denture looseness:

a. Denture faults:
 1. Incorrect peripheral extension.
2. Teeth not in neutral zone.
3. Unbalanced articulation.
4. Polished surface is unsatisfactory.
b. Patient’s factors:
1. Inadequate volume of saliva.
2. Poor ridge form.
3. Lower adaptive skills.

Burning mouth from dentures:

1. Local causes: (e.g increased OVD, sensitivity to acrylic monomer,

candidiasis or mouthwashes).
2. Systemic causes: (e.g menopause, deficiency state, xerostomia,
cancerphobia.

Causes of pain from dentures:

1. Roughness of the fitting surface.

2. Errors in occlusion.
3. Lack of FWS.
4. Bruxing habit.
5. Retained root or any other pathology.
6. Premature contact.
7. Pressure on the mental foramen from continued resorption.
8. Overextension.

Pain from an individual tooth in P/P:

1. Excessive load or traumatic occlusion.

2. Leverage due to unstable denture.
3. Clasp arms are too tight.
4. Inadequate lining under amalgam (galvanic couple with denture metal
base).

Retching:

1. Map out extent of sensitive area on palate using a ball-ended instrument

and check extension of the dentures.
 2. Palateless dentures (although poorly retentive).
3. Training dentures.
4. Hypnosis.
5. Implant.

Solutions for resorbed lower ridge:

1. Minimize destabilizing forces:

a. Maximum extension of denture base.
b. Reduce number and width of teeth.
c. Increase FWS.
d. Lower occlusal plane.
2. Neutral zone impression technique.
3. Surgery.
4. Implants.

Denture induced stomatitis:

F>M = 4:1

Causes:

1. Poor denture hygiene.

2. Infection with candida.
3. Night-time wear.
4. Trauma.
5. Systemic factors:
a. Iron deficiency.
b. Vitamin deficiency.
c. Steroids.
d. Drugs which cause xerostomia.
e. And endocrine abnormalities.
f. High sugar intake.

Management:

1. Remove denture at night.

2. Cleaning dentures thoroughly, brushing fitting surface and soaking in
hypochlorite solution.
 3. New denture can be made.
4. Reduce sugar intake.
5. Miconazole gen can be added to the fitting surface of the denture.
6. Systemic fluconazole may be used.
7. Refer to GMP for suspected systemic factor.

Risk factors of implant placement:

1. Smoking
2. Untreated periodontal disease.

Possible C/I

1. Poorly controlled D.M.

2. Immunosuppression.
3. Scleroderma.
4. Bisphosphonates.

Bone augmentation:

1. Onlay grafting
a. Autogenous bone grafts.
b. Allograft.
c. Xenografts.
2. Ridge expansion.
3. Sinus elevation.
4. Distraction osteogenesis.

TMJ ligaments:

1. Sphenomandibular ligament  pivot of the mandible, maintaining the

same amount of tension during opening and closing.
2. Stylomandibular ligament  limit anterior protrusion of the mandible.
3. Lateral ligament  prevents lateral and posterior displacement.

Side effects of mouth wash use:

1. Ulcerative erosions.
2. Staining of teeth and tongue.
3. Burning sensation.
 4. Disturbed taste sensation.
5. Dry mouth.

TMJ capsule attachment:

1. Superior: along the rim of the temporal articular surfaces.

2. Inferior: along the condylar neck.
3. Medial: Blends along the medial collateral ligament.
4. Lateral: blends along the lateral collateral ligament.
5. Anterior: blends with the superior head of the lateral pterygoid muscle.
6. Posterior: along the retrodiscal pad.

Blood supply of TMJ:

1. Deep auricular (maxillary artery).

2. Anterior tympanic (maxillary artery).
3. Superficial temporal (terminal branch of ECA).

Sensory nerves of TMJ:

1. Auriculotemporal.
2. Masseteric
3. Posterior deep temporal

What is MIH?

It is a developmentally derived dental defect that involves hypo mineralization

of 1-4 first permanent molars, frequently associated with similarly affected
permanent incisors.

Management of MIH:

1. Prevention: Flouride tooth paste, fluoride varnish 2.2%, fluoride mouth

rinse, dietary analysis.
2. Stabilization: GIC, referral to orthodontist for retention of first permanent
molars.
3. Sensitivity: Flouride mouth wash, varnish, Casein phosphopeptide-
Amorphous calcium phosphate, CPP-ACP, tooth mousse.
4. Nitrous oxide + articaine.
5. Fissure sealant.
 6. Restorations.

Signs of impacted upper canines:

1. Absence of upper 3s.

2. Absence of palpable bulge in buccal sulcus.
3. Cs still in place.
4. Protrusion of lateral incisors.
5. Hypodontia or absent upper 2s.

When to extract impacted upper 3s?

1. When the tooth shows pathology associated with it (cyst or resorption).

2. Root resorption.
3. Orthodontic treatment is planned and upper canines are interfering.
4. Implant.

When not to extract impacted upper 3s?

1. When patient declines treatment.

2. No pathology.
3. No orthodontic treatment is planned.
4. Risk of damaging adjacent teeth/tooth.
5. Contraindications in medical history.

Adams’ clasp:

1. Easy to adjust.
2. Provides both anchorage and retention.
3. Versatile: auxiliary fittings including double clasps, hooks for elastic tubes
for headgear attachment.

Delayed eruption of primary teeth:  1%

1. Preterm birth.
2. Nutritional deficiency.
3. Hereditary gingival fibromatosis.
4. Chromosomal abnormalities, eg Down syndrome, Turner syndrome.

Delayed eruption of permanent teeth:  3.5-6.5%

 1. Local:
a. Supernumerary teeth.
b. Crowding.
c. Cystic change around the follicle.
d. Ankylosed primary teeth.
e. Ectopic position of tooth germ.
2. Systemic:
a. Nutritional deficiency.
b. Hereditary Gingival fibromatosis.
c. Chromosomal abnormalities.
d. Cleidocranial dystostosis.
e. Hypothyroidism.
f. Hypopitutirism.

Splinting time:

1. Avulsion  1-2 weeks.

2. Mid-third root fracture  4 weeks.
3. Coronal third root fracture  3-4 months (I think rigid, need to check)
4. Alveolar bone fracture  4 weeks.
5. Luxation  2-3 weeks.

Band and loop  0.8 mm

Types of space maintainers:

1. Band and loop.

2. Distal shoe.
3. Lingual arch.
4. Nance appliance (maxillary arch)

Space regainer is indicated when space loss is < 3mm

Types of space regainers:

1. Removable appliance with finger springs.

2. Headgear (for maxillary teeth)
3. Activated lingual arch (for mandibular teeth).
 4. Lip bumper.
5. Limited fixed appliance.

Radiotherapy:

1. Mucositis.
2. Xerostomia:
a. Dysphagia.
b. Caries.
c. Disturbed taste.
d. Candidosis.
e. Bacterial sialadenitis.
3. ORNJ
4. Trismus

Crohn’s:

1. Facial and labial swelling.

2. Angular stomatitis.
3. Ulcers.
4. Mucosal tags.
5. Cobblestone appearance of the buccal mucosa.
6. Gingival hyperplasia.
7. Cheilitis.
8. Melkersson-Rosenthal syndrome: lip or facial swelling in combination
with fissured tongue and LMN facial palsy.

Skin lesions of LP:

1. Itchy, purple, polygonal papules in the wrists (Koebner’s)

2. Ridging of nails.
3. Alopecia.
4. Genital erosions.

Lesions associated with HIV:

1. Strong association:
a. Candidiasis.
b. Hairy leukoplakia.
 c. Kaposi’s sarcoma.
d. NUG.
e. Periodontitis.
f. Gingivitis.
g. Non-Hodgkin’s lymphoma.
2. Less common association:
A. Oropharyngeal ulceration.
B. ITP.
C. Dry mouth.
D. Viral infections:
I. CMV.
II. HSV.
III. HPV.
IV. VZV.

Acquired lip swelling:

1. Inflammatory:
a. Infections.
b. Bites.
c. Crohn’s disease.
d. Orofacial granulomatosis.
e. Sarcoidosis.
2. Immunological: Allergy, angioedema.
3. Traumatic: oedema, haematoma.
4. Cysts.
5. Hamartomas.
6. Neoplasms.
7. Systemic CS.
8. Cushing’s syndrome.

Chapping of lips:

1. Dehydration.
2. Hot dry winds.
3. Fever.
4. Cheilitis.
 5. Erythema multiforme.
6. Drug.
7. Psychogenic.

Causes of angular stomatitis:

1. Denture stomatitis.
2. Inadequate vertical dimension.
3. Immune deficiency: diabetes, HIV
4. Nutritional deficiency: riboflavin, iron, vitamin B.

What happens if implant was placed too deep?

1. Bone resorption.
2. Peri-implantitis.
3. Increased stress on implant-abutment interface.
4. Possible damage of vital sturctures.

What happens if implant was placed too shallow?

1. Metal may show.

2. Threads are plaque retentive  periimplantitis.
3. No enough space for abutment.
4. Emergence profile is difficult to form.

Implant head should be 3 mm below gingival margin.

1.5 mm between tooth and implant, 3-4 mm between implants, to preserve

interdental papilla.

What happens if implant positioned too labial?

Bone resorption with recession

What happens if implant positioned too lingual?

1. Compromise aesthetics.
2. Hinder plaque control.
3. Unfavourable load dissipation.

Functions of saliva:
 1. Acid buffering.
2. Digestion.
3. Antibacterial action (lysozyme, IgA, lactoferrin)
4. Facilitate eating and speech.
5. Dilution and clearance.

Signs and symptoms of hypoglycaemia:

1. Excitability.
2. Irritability.
3. Drowsiness.
4. Disorientation.
5. Hunger.
6. Wet skin.
7. Blurred vision.
8. Irrational behaviour (mistaken for drunkenness).
9. Paraesthesia of extremities.

Articular disk:

Meniscus is a sheet of CT rich in sulfated GAG. Soft peripheral zone of the

meniscus is composed of a loose connective tissue receiving blood supply and
innervation.

Synovial fluid  produced by synovial cells and acts as a lubricant, contributes

to nutrition of avascular parts of condyle, fossa and disc.

Gingival swelling:

1. Localized:
a. Crohn’s
b. Oro-facial
c. Sarcoidosis.
d. Wegner’s granulomatosis (strawberry enlargement of gingiva)
e. Pyogenic granuloma.
f. GCG.
g. Fibro-epithelial polyp.
h. Carinomas.
i. Lymphomas.
 2. Generalized:
a. Periodontal disease.
b. HGF.
c. Drug.
d. Leukaemia.
e. Vitamin C.
f. Sarcoidosis.
g. Crohn’s.
h. Orofacial.

Causes of facial palsy:

1. UMN:
a. CVA.
b. Trauma.
c. Tumour.
d. Infection.
e. MS
2. LMN:
a. Infection: Bell’s palsy, VZV, HIV, lyme disease.
b. Middle ear infections.
c. Lesions of skull base.
d. Parotid lesion.
e. Trauma to the nerve.
f. Local anaesthesia

Causes of enlarged LN:

1. Infection:
a. Bacterial: TB, syphilis.
b. Viral: EBV, CMV, HHV-6, HIV.
2. Inflammatory:
a. Sarcoidosis.
b. Crohn’s.
3. Neoplastic:
a. Leukaemia
b. lymphoma
 4. Metastatic

Parts of the facebow:

1. 2 arms.
2. 2 ear plugs.
3. Pointer.
4. Reference plane locator.
5. Bite fork.
6. Platform.
7. Swivel for assembly.

Risk factors of oral candidiasis:

1. Faulty dentures.
2. Immunosuppression: diabetes, HIV, steroid.
3. Smokers.
4. Abx.
5. Xerostomia.
6. Malignancy (radiotherapy/chemotherapy)

RAS types:

1. Major: single. >10 mm, 5-10 weeks. Keratinized mucosa. Scarring, seen in
AIDS
2. Minor: multiple 1-6. 2-5 mm, 1-2 weeks. Non-keratinized mucosa. No
scarring.
3. Herpetiform: multiple 100, 1-2 weeks. Non-keratinized and keratinized.
Scarring if multiple ulcers merge.

Treatment of pemphigus:

1. Systemic CS.
2. Azathioprine.
3. Dapsone.
4. Cyclophosphamide.

Trigger factors of EM:

1. Drugs: (sulphonamides, barbiturates, NSAIDs)

 2. HSV, mycoplasma.
3. Pregnancy
4. Malignancy.
5. Sunlight
6. Chemicals.

Addison’s disease  low BP, low Na, low cortisol level and response to ACTH
stimulation (Synacthen test)

Histopathological features of dysplasia:

1. Thick surface layer of keratin.

2. Thickening of prickle cell layer.
3. Acanthosis.
4. Cellular atypia.
5. Nuclear hyperchromatism.
6. Nuclear pleomorphism.
7. Increased nuclear/cytoplasmic ratio.
8. Atypical mitosis.

Factors that govern the management of leukoplakia:

1. Degree of dysplasia.
2. Site.
3. Relation to the cause.

Submucous fibrosis:

Copper due to areca nut chewing  increased cross-linking of collagen 

fibrosis and DNA damage.

Management of premalignant lesions:

1. Photographic records.
2. Smoking cessation.
3. Guided biopsy with toluidine blue.
4. Laser excision.
5. Cryotherapy.
6. Surgical excision.
7. Vitamin A therapy.
 8. Retinioids.
9. Follow-up at 3 month intervals.

HP of LP:

1. Hyperparakeratosis.
2. Liquefactive degeneration of basal cell keratinocytes.
3. Presence of Civatte bodies.
4. Intra- and sub-epithelial T-lymphocytic infiltration.
5. Saw-tooth rete ridges.

Rx of LP:

1. Explanation and reassurance.

2. Biopsy to exclude malignancy.
3. Betamethasone 1 mg rinsed for 3 minutes tds or qds.
4. Prednisolone mouthwash.
5. Topical dexamethasone.
6. In severe cases: oral steroids, azathioprine, tacrolimus.
7. Erosive LP should be reviewed every 6 months to exclude malignant
transformation.
8. Clinical photography and repeat biopsy may be indicated.

Oral features of anaemia:

1. RAS.
2. Angular cheilitis.
3. Glossitis.
4. Burning mouth syndrome.
5. Candidiasis.

Oral features of leukemia:

1. Candidiasis.
2. Herpetic infections.
3. Bleeding and petechial haemorrhage.
4. Gingival swelling, ulceration and mucosal pallor.

Oral features of D.M:

 1. Candidiasis.
2. Xerostomia.
3. Lichenoid reaction.
4. Burning mouth syndrome.
5. Oral dysesthesia.

Space maintainer gauges:

1. Distal shoe  0.04 inch  1 mm

2. BLS  0.036 inch  0.8 mm

Types of space maintainers:

1. BLS.
2. Distal shoe.
3. LLHA.
4. PHA.
5. Nance appliance (acrylic button added).
6. Removable appliances.

Strabismus/ocular misalignment

Esotropia  caused by unopposed action of medial rectus, causing adduction of

the eyeball towards the nose

Uses of Botulinum toxin in dentistry:

1. Aesthetic surgeries to reduce wrinkles.

2. Trismus.
3. Gustatory sweating.
4. Gustatory lacrimation.
5. Drooling.
6. Torticollis.
7. Blepharospasm.

Free gingiva  the mot coronal portion of the gingiva, extending from the free
gingival margin to the free gingival groove (FGM-FGG) = 0.5-3mm
Attached gingiva  firmly bound to underlying cementum and bone, extends
from FGG-MGJ, usually narrower on the lingual aspect of lower incisors and
labial aspect of canines and first premolars, width increases with age.

MGJ  junction of keratinized and non-keratinized mucosa.

Schiller iodine solution  distinguishes keratinized from non-keratinized

mucosa, useful to determine the width of keratinized tissue in gingival recession.

Keratinized  orange.

Non-keratinized  purple-blue.

PDL space  0.1-0.2 mm on x-rays.

Factors that may lead to error in measuring probing depth:

1. Thickness of probe.
2. Contour of tooth surface.
3. Angulation of probe.
4. Pressure applied.
5. Presence of calculus deposits.
6. Presence of inflammation.

NUG clinical features:

1. Punched out ulcers with yellow-grey pseudomembraneous slough.

2. Interdental papillae affected first.
3. Pain.
4. Halitosis
5. Metallic taste.

Bacteria that cause NUG:

1. Gram -ve anaerobic  Porphyrmonas gingivalis, Veillonella, Selenomona

spp.
2. Fusi-spirochaetal complex (red complex)  fusobacterium nucleatum,
Boreilla vencenti, Boreilla Burgdorferi.

Risk factor of NUG:

1. Poor plaque control.

 2. Smoking.
3. Mental stress.
4. Malnutrition.
5. HIV.
6. Immunoupression.

Management of NUG:

1. Smoking cessation advice.

2. OHI.
3. Debridement (with or without L.A)
4. Metronidazole 200 mg tds for 3 days.
5. Oxygenating mouth wash (hydrogen peroxide, sodium hydroxyperborate)

Stillman’s cleft

McCall’s Festoon  canines on labial side when recession approaching MGJ

Treatment of gingival recession:

1. Record the magnitude of recession.

2. Eliminate etiological factor.
3. OHI.
4. Flouride varnish if there’s sensitivity.
5. Mucogingival surgery.
6. Gingival veneer.

Gingival enlargement associated with drugs:

Phenytoin  50%

Cyclosporine  30%

Nifedipine  20%

Epulis  localized hyperplastic lesions arising from the gingiva caused by chronic
irritation from plaque and calculus invoking a chronic inflammatory response.

PLS, EDS, LADS, LCH

Retention: Resistance of a denture to vertical movement away from the tissues.

Stability: Resistance of a denture to displacement by functional forces.

Causes of reduced stability:

1. Flabby ridge.
2. Unsupported ridge.
3. Extensive resorption.
4. Inadequate muscle control.

Benefits of beading of impressions:

Provide a land area to protect the width of the sulcus on the resultant cast.

Contraction porosity  insufficient acrylic dough, insufficient pressure.

Gaseous porosity  temperature of dough raised above boiling point of

monomer (100C), producing spherical voids (lingual flanges of lower dentures).

Granular porosity  incorrect powder-liquid ratio, incorrect manipulation or

mixing, loss of monomer.

Hypodontia  3.5-6.5%

Male:female = 1:1.4

Syndromes associated with hypodontia:

1. Ectodermal dysplasia.
2. Clefting.
3. Down syndrome.
4. Chondro-ectodermal dysplasia.
5. Reiger syndrome.
6. Orofacial digital syndrome.

Supernumerary  1.5-3.5%

Male:female = 2:1

Syndromes associated with supernumeraries:

1. Cledocranial dysostosis.
2. Gardner’s syndrome.
3. Clefting.
 4. Orofacial digital syndrome.

AI:

1. Hypoplastic.
2. Hypomineralized: hypocalcified or hypomatured.

Hypoplastic AI : deficient matrix production but enamel is properly mineralized

 pitting and grooving.

Hypocalcified AI: enamel is dull, lustreless, opaque white or honey coloured.

Hypomaturation AI: Similar to hypocalcified but with no normal enamel in

cervical region.

Gingival hyperplasia due to drug mechanism: Proliferation of subgingival

collagen mainly of the interdental papillae which become grossly swollen, pale
and firm.

Leeway space  difference between the width of primary canine and molars
and the width of permanent canine and premolars.

In upper arch  1 mm on each side.

In lower arch  2.5 mm on each side.

Cephalometric values:

• SNA = 81±3
• SNB = 78±3
• ANB = 3±2
• Upper 1 to maxillary plane = 109±6
• Lower 1 to mandibular plane = 93±6
• Interincisal angle = 135±10
• MMPA = 27±4

Hypodontia:

1. Third molars  25-35%

2. Lower second premolars  3%
3. Upper lateral incisors 2%
 4. Lower incisors 0.2%

CLP incidence  1:750

Isolated cleft in the secondary palate  1:2000

Syndrome associated with CLP:

1. Pierre Robing.
2. Treacher-Collins.
3. Down syndrome.

Skeletal features in CLP:

1. Class III from maxillary deficiency.

2. Reduced UFH, increased LFH, increased freeway space.

Dental features of CLP:

1. Lateral incisors are absent, abnormal size and shape, hypoplastic.

2. Supernumerary teeth.
3. Central incisors are often rotated.

Factors in determining treatment plan for anterior cross bite:

1. Overbite.
2. Whether patient can achieve edge-to-edge contact.
3. Angulation of upper incisors.
4. Angulation of lower incisors.
5. Amount of space available.

Factors that may favour orthodontic alignment of upper 3 impacted:

1. General factors, motivation.

2. Presence of space.
3. Below apical third of incisors, overlapping less than half the MD width of
upper 1, less than 30 degrees to midsagittal plane and apex not distal to
5.

Factors to consider in space maintenance:

 1. Amount of resorption in primary roots (more than ¼ remains  space
maintenance necessary.
2. Amount of bone covering the tooth.
3. Root development  bone pierced when 2/3 of root is completed,
gingival tissue is pierced when ¾ root formation is completed.
4. Eruption of neighbouring teeth, if erupted less space loss occurs.
5. Time since loss.
6. Patient’s age, rule of 7, eruption of premolars is delayed if exfoliation is
before 7. Accelerated if loss occurs after 7.
7. Delayed or deviant eruption. Ectopic eruption of upper 6s.

Oral features of xerostomia:

1. Difficulty in talking.
2. Difficulty in swallowing.
3. Altered taste.
4. Unretentive dentures.
5. Generalized erythema.
6. Lobulated dorsum of the tongue.
7. Predisposition to infection:
a. Angular cheilitis.
b. Oral candidiasis.
c. Cervical caries.
d. Recurrent caries around restorations.
e. Ascending sialadenitis.

Carlsson-Crittenden cup  collects saliva from individual salivary glands.

D.Dx of white lesions:

1. Neoplastic:
• Leukoplakia.
• SCC.
• Keratosis.
2. Inflammatory:
• Lichen planus.
 • SLE.
• DLE.
3. Infections:
• Viral: hairy leukoplakia.
• Candidiasis.
• Papilloma.
4. Congenital:
• White sponge neavus.
• Fordyce spots.
• Leukodema.
5. Others
• Cheek biting.
• Frictional keratosis.
• Burns.
• Grafts.

Lichenoid drug reaction:

Predisposing factor:

1. Drugs: antimalarials, antidiabetics, antihypertensive, NSAIDs, gold salts,

allopurinol.
2. Amalgam and gold restorations.
3. GVHD.
4. HBC and chronic liver disease.

Histopathological features of dysplasia:

1. Nuclear pleomorphism.
2. Increased nuclear:cytoplasmic ratio.
3. Suprabasal mitoses.
4. Increased number of nucleoli.
5. Loss of polarity of cells.
6. Bulbous rete process.
7. Nuclear hyperchromatism.
8. Loss of cellular cohesion.

Drugs that cause xerostomia:

 1. TIA.
2. Antidepressants.
3. SSRI.
4. Atropine and hyoscine.
5. Anti-reflux agents.
6. Antihistamines.
7. Opioids.
8. Diuretics.

L.A overdose signs and symptoms:

1. CNS:
• Light-headedness.
• Dizziness.
• Circumoral paraesthesia.
• Visual and auditory disturbance.
• Tinnitus.
• Disorientation.
• Drowsiness.
• Shivering.
• Muscle twitching.
• Tremor.
2. CVS:
• If there’s adrenaline: Tachycardia, Increased blood pressure.
• If not adrenaline: hypotension and bradycardia.

HP features of GCG:

1. Giant cells (osteoclasts).

2. Vascular stroma (connective tissue).
3. Spindle-shaped cells.
4. Haemosiderin.
5. Fibroblasts.
6. Osteoid.

Why does OKC recur?

 1. Fragile cyst lining.
2. Daughter cysts.
3. Multi-locular and finger like extension.
4. Rapid proliferation.
5. Remnant of dental lamina may produce more lesions.

HP of OKC:

1. Uniform thickness of epithelium.

2. Flat basement membrane, 5-10 cells.
3. Elongated palisaded basal cells.
4. Folded cyst lining.
5. Thin fibrous wall.
6. Orthokeratin formation.

HP of LP:

1. Hyperparakeratosis.
2. Saw-tooth rete ridges.
3. Band-like lymphocytic infiltration in the juxta-epithelial lamina propria.
4. Lymphocytic infiltration into basal cell layers of the epithelium and CD8.
5. Hyaline or Civatte bodies in epithelium.
6. Oedema in basal cell layers resulting in liquefactive degeneration of the
basal cell layer.

Side effects of mouth wash:

1. Tooth staining.
2. Burning sensation
3. Disturbed taste sensation.
4. Parotid swelling.
5. Dry mouth.
6. Desquamative gingivitis.
7. Mucosal erosions.

Treatment protocol for Peri-implantitis:

1. Protocol A: Probing depth < 3 mm, plaque, bleeding on probing  OHI +

mechanical cleaning with air-powder-abrasive system.
 2. Protocol B: Probing depth 4-5 mm  chlorhexidine gel, mouthwash and
irrigation.
3. Protocol C: Probing depth >5mm  systemic antibiotic for 10 day
(metronidazole and/or amoxicillin).
4. Protocol D: Probing depth > 5mm + bone loss  surgical treatment such
as GTR + OHI + debridement.

Factors governing the balanced occlusion:

1. Incisal guidance.
2. Condylar guidance.
3. Prominence of the compensating curve.
4. Cusp angles of posterior teeth.
5. Orientation of the occlusal plane.
MFD Part II December 2016:

The exam was easier than expected (not too easy, it requires extensive studying
but there wasn’t anything ambiguous, the examiners were very helpful.

1. CPR Station:
a. Tell the examiner that you will check the surrounding for danger and
whether the scene is safe to approach the victim.
b. Shout and shake (can you hear me?)
c. Chin lift and head tilt, check breathing for 10 seconds.
d. No response  tell the examiner that you will call for help, and that
you will tell them the following information:
• A cardiac arrest is suspected.
• You name.
• You telephone number.
• Your address.
e. Start compressions 30:2.
f. The examiner stops you after 2 or 3 cycles and asks when do you stop?
• If I get exhausted.
• Help arrive.
• The patient recover.
g. Examiners asks how many compressions per minute? 100-120.
h. Describe recovery position.
i. What is its importance? To prevent rolling of the patient and to keep
the airway clear from secretions and saliva.
2. Place rubber dam on a lower left second premolar for class II restoration,
make 3 holes and choose your clamp, it’s a good practice to tie your clamp
with a piece of floss, try the clamp on if it fits then proceed. The examiner
liked it, don’t forget to push rubber dam through the contacts, the
examiner appreciates accuracy.
3. Cranial nerve examination, was easier than I thought, the examiner will
ask you questions and guide you throughout the examination.
4. Cephalometric analysis, points A, B, Maxillary plane, mandibular plane,
with their definition, what cephalometric changes would you expect to
see after treatment with Medium opening activator?
5. Case of RPD picture of an RPD design, Kennedy Class I in the lower arch, it
was continuous cingulum and lingual bars, what are the advantages of this
type of bar? Indirect retention, increased stability and support, addition
of teeth is easier in case one of the natural teeth is extracted. How can
you improve the support and retention from distal extension RPD?
Maximum coverage of the distal extensions, use of smaller and fewer
teeth, use of indirect retention, use of RPI system.
6. Suturing, Vertical, horizontal and simple interrupted, just dispose of your
needle after you finish, practice and practice is my advice for this.
7. Red lesion on the lingual surface of anterior mandible with indurated
margins, what histological features are expected? Dysplasia. What factors
other than the histological that can provide you with a clue of the
prognosis? Size, lymph nodes, metastasis, gender, location. What are the
causes of this lesion? Smoking, alcohol, malnutrition, HPV.
8. Fibroma in the cheek with histological section, describe what you see and
give three differential diagnoses.
9. WHO probe, mention the grading, they gave us BPE score and treatment
needed for a case with many pockets in upper left sextant from upper left
4 to upper left 8, all pockets were below 6 mm except on the 8 which
doesn’t count, so it’s BPE =3, many candidates have written 4 which is
wrong, treatment needed are the three, OHI, scaling, root surface
instrumentation for all pockets 3.5-5.5 mm
10.Picture of the TMJ ligament, name these ligaments? Lateral TMJ ligament,
sphenomandibular, stylomandibular. What are the sensory innervation of
the TMJ? Auriculotemporal nerve if he asks for motor you would say
posterior deep temporal and massetric. What are the functions of the
disc? I made this answer up.
11. Trauma to a deciduous tooth, can’t remember the whole question, it was
luxation injury.
12. Name these signs, latex allergy, single use, radiation hazard, what are the
advantages of vaccum over non-vaccum autoclaves (Old chestnut) and
what are the temperatures, times and pressures used.
13. X-ray showing a tooth with external resorption, what are the types of
tooth resorption? If you want to have it treat it with a post, what are the
guidelines for the length? (4 points) and width of the post core?(3 points).
 14.Forgot this one, but if I remember I will tell you.
15.Forgot this one,
16.Rest station.
17.Rest station.

VIVA: