Oral Pathology and Oral Medicine I: Main Exam, 10 November 2025

Mount Kenya University · Department of Dental Sciences · Diploma in Dental Technology · DDS2107

Oral Pathology and Oral Medicine I (DDS2107) Mount Kenya University 2025-2026 main exam with model answers.

Instructions: ATTEMPT ALL QUESTIONS IN SECTION A AND ANY TWO IN SECTION B

SECTION A (30 marks)

1. Explain the process of describing a pathological condition. (8 marks)

Model answer
  • Observation: Identify lesion location, size, shape, colour, surface texture and relationship to surrounding structures.
  • History: Record patient’s age, sex, duration, symptoms, habits, systemic conditions and precipitating factors.
  • Clinical description: Use standardized terminology (e.g., ulcer, papule, plaque) and describe margins (well/ill‑defined), base (smooth, indurated), exudate and pain.
  • Differential diagnosis: List possible conditions based on the description.
  • Investigations: Note any radiographs, biopsies, microbiology or laboratory tests required.
  • Final diagnosis: State the most probable pathological condition with justification.
  • Management plan: Outline treatment options, prognosis and follow‑up.
  • Documentation: Record all findings clearly in the patient’s chart for future reference.

2. Explain the etiology of developmental abnormalities of the face and oral cavity. (8 marks)

Model answer
  • Genetic factors: Chromosomal anomalies (e.g., trisomy 13, 18) and single‑gene mutations affecting craniofacial development.
  • Teratogenic exposures: Maternal use of alcohol, retinoids, anticonvulsants or radiation during the first trimester.
  • Nutritional deficiencies: Lack of folic acid, vitamin A or essential minerals during embryogenesis.
  • Infections: Maternal rubella, cytomegalovirus, toxoplasmosis or syphilis disrupting facial process formation.
  • Mechanical forces: Amniotic band syndrome causing constriction and tissue loss.
  • Endocrine disturbances: Maternal diabetes mellitus leading to altered neural crest cell migration.
  • Environmental factors: Maternal smoking, high altitude hypoxia or exposure to heavy metals.
  • Maternal systemic disease: Autoimmune conditions (e.g., lupus) affecting placental function.
  • More answers: epigenetic alterations, maternal drug abuse, nutritional excess (vitamin A toxicity), infections like herpes simplex, and maternal stress hormones.

3. Differentiate between hyperplasia and hypertrophy of oral cavity tissues. (7 marks)

Model answer
  • Hyperplasia: Increase in the number of cells in a tissue; the cells remain normal in size and retain normal architecture.
  • Hypertrophy: Increase in the size of existing cells; cell number does not change markedly.
  • Stimulus: Hyperplasia is usually a response to chronic irritation or hormonal stimulation; hypertrophy occurs when functional demand on the tissue rises (e.g., masticatory overload).
  • Reversibility: Both are reversible; removal of the stimulus leads to a reduction in tissue mass.
  • Histology: Hyperplastic tissue shows more cell layers; hypertrophic tissue shows enlarged cytoplasm and nuclei.
  • Clinical example: Hyperplasia – gingival overgrowth from phenytoin; Hypertrophy – enlarged masseter muscle in bruxism.
  • More answers: hyperplasia may involve increased stromal components, hypertrophy may involve increased organelle content, and both can coexist in the same lesion.

4. Outline the results from failure of fusion of facial processes. (7 marks)

Model answer
  • Cleft lip: Failure of fusion between the medial nasal and maxillary processes results in a unilateral or bilateral cleft of the lip.
  • Cleft palate: Incomplete fusion of the palatine shelves leads to a hard and/or soft palate defect.
  • Facial asymmetry: Unequal growth of the maxillary processes produces midline deviation and asymmetrical facial appearance.
  • Nasolabial fistula: Persistent communication between oral and nasal cavities due to incomplete fusion of the nasolabial groove.
  • Dental anomalies: Missing, malformed or ectopic teeth in the region of the cleft.
  • Speech and feeding problems: Result from palate defects affecting articulation and ability to generate suction.
  • More answers: submucous cleft palate, alveolar ridge discontinuity, and associated ear infections due to eustachian tube dysfunction.

SECTION B

5. Discuss the classification and clinical significance of oral ulcers. (20 marks)

Model answer
  • Classification by aetiology
  • Traumatic ulcers: caused by mechanical injury, burns or iatrogenic trauma.
  • Infectious ulcers: viral (herpes simplex, Coxsackie), bacterial (syphilis, tuberculosis), fungal (candidiasis).
  • Immune‑mediated ulcers: aphthous stomatitis, pemphigus vulgaris, mucous membrane pemphigoid.
  • Neoplastic ulcers: malignant transformation of leukoplakia or carcinoma presenting as non‑healing ulcer.
  • Drug‑induced ulcers: NSAIDs, chemotherapeutic agents causing mucosal necrosis.
  • Classification by duration
  • Acute ulcer: <2 weeks, usually self‑limiting.
  • Chronic ulcer: >2 weeks, warrants biopsy.
  • Classification by depth
  • Superficial ulcer: involves epithelium only; painful, heals quickly.
  • Deep ulcer: extends into lamina propria or muscle; may scar.
  • Clinical significance
  • Diagnostic clue: pattern, location and pain help narrow differential diagnosis.
  • Risk of malignancy: persistent non‑healing ulcers >3 weeks may indicate squamous cell carcinoma.
  • Impact on nutrition: painful ulcers impair eating, leading to weight loss.
  • Infection risk: ulcerated mucosa provides portal for secondary bacterial infection.
  • Quality of life: chronic pain affects speech, sleep and psychosocial wellbeing.
  • Management implications: etiology‑directed therapy (antivirals, steroids, surgical excision) and need for follow‑up biopsies.
  • Prognosis: depends on cause; traumatic ulcers heal fully, whereas malignant ulcers have guarded prognosis.
  • More answers: classification by location (labial, dorsal tongue, floor of mouth), by size (minor <5 mm, major >5 mm), and by recurrence pattern (recurrent aphthous vs. solitary).

6. Explain the four (4) types and clinical features of periodontal diseases. (20 marks)

Model answer
  • Chronic marginal (gingivitis) disease
  • Clinical features: red, swollen gingiva; bleeding on probing; no loss of attachment.
  • Chronic periodontitis
  • Clinical features: pocket formation >4 mm, clinical attachment loss, alveolar bone resorption, tooth mobility.
  • Aggressive periodontitis
  • Clinical features: rapid attachment loss, familial aggregation, often in otherwise healthy young patients; minimal plaque.
  • Necrotizing periodontal disease
  • Clinical features: necrotic papillae, ulcerated gingival margins, pseudomembrane formation, severe pain, fetid breath; associated with immunosuppression or stress.
  • More answers: systemic forms (periodontitis as manifestation of systemic disease), peri‑implantitis, and pregnancy‑associated gingivitis.

7. Explain the general factors affecting structural defects of teeth. (20 marks)

Model answer
  • Genetic factors – inherited anomalies (e.g., dentinogenesis imperfecta, amelogenesis imperfecta) determine enamel/dentin quality and tooth size.
  • Developmental timing – disturbances during bud, cap or bell stage cause hypoplasia, enamel pits or missing teeth.
  • Nutritional deficiencies – lack of calcium, vitamin D or protein during odontogenesis leads to enamel hypomineralisation and reduced dentine formation.
  • Systemic illnesses – high fever, rubella, measles or maternal infections during pregnancy can disrupt ameloblast/odontoblast activity.
  • Teratogenic drugs – tetracycline, thalidomide, retinoids or excessive fluoride exposure interfere with mineralisation and cause enamel defects.
  • Trauma to primary teeth – impact or intrusion of a deciduous tooth can damage the developing permanent tooth bud, resulting in enamel hypoplasia or root malformation.
  • Local infections – periapical or periodontal infections of primary teeth may alter the follicle of the succedaneous tooth.
  • Radiation exposure – therapeutic or accidental radiation to the head/neck region during tooth development impairs cell proliferation and matrix formation.
  • Metabolic disorders – endocrine abnormalities (e.g., hyperparathyroidism) affect calcium/phosphate balance, leading to structural weaknesses.
  • Environmental pollutants – exposure to lead, dioxins or high levels of fluoride (fluorosis) can produce enamel mottling and hypoplasia.
  • Nutritional excesses – excessive fluoride intake during enamel formation causes dental fluorosis, a structural defect.
  • Maternal health – maternal malnutrition, diabetes or drug abuse can impair fetal odontogenesis.
  • Genetic‑environment interaction – epigenetic modifications may exacerbate inherited susceptibility to structural defects.
  • Age of exposure – earlier insults (bud stage) produce more severe defects than later (root formation).
  • Severity and duration of insult – prolonged or repeated exposure leads to larger areas of hypoplasia or hypomineralisation.
  • Location within the arch – anterior teeth are more susceptible to certain defects (e.g., fluorosis) due to earlier eruption.
  • Oral hygiene and bacterial colonisation – early colonisation can exacerbate enamel breakdown in already compromised structures.
  • Socio‑economic factors – limited access to nutrition and healthcare increases risk of developmental defects.
  • Caries‑induced structural loss – while not a developmental defect, secondary caries can mimic structural defects and further weaken tooth integrity.
  • Post‑eruption wear – attrition and abrasion can accentuate pre‑existing developmental defects, making them clinically apparent.

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