Oral Biology II: Main Exam, 20 November 2024

Mount Kenya University · Department of Dental Sciences · Diploma in Community Oral Health · DDS2212

Oral Biology II past paper from Mount Kenya University 2024-2025 with model answers for each question.

Instructions: ATTEMPT ALL QUESTIONS IN SECTIONS A AND B

SECTION A : 30 MARKS (30 marks)

1. Explain the chemical composition of enamel and dentin. (10 marks)

Model answer
  • Hydroxyapatite crystals: ~96% of enamel by weight, providing hardness and mineral content.
  • Water: ~2% of enamel, present in the crystal lattice and intercrystalline spaces.
  • Organic matrix: ~2% of enamel, mainly amelogenins, enamelins and tuftelin, essential for crystal growth.
  • Dentin mineral: ~70% hydroxyapatite, giving rigidity.
  • Dentin organic matrix: ~20% collagen type I fibers, plus non‑collagenous proteins (DSP‑P, DMP‑1) that regulate mineralisation.
  • Dentin water: ~10% of dentin, occupies tubules and interfibrillar spaces.
  • Differences: Enamel lacks collagen and tubules, is more highly mineralised; dentin has a collagenous scaffold and dentinal tubules for nutrient transport.

2. Outline the factors which increase the absorption of calcium intake. (6 marks)

Model answer
  • Vitamin D status: enhances intestinal calcium absorption by up‑regulating calbindin.
  • Dietary calcium source: soluble salts (e.g., calcium citrate) are absorbed more efficiently than insoluble forms.
  • Low dietary phytate/oxalate: these bind calcium and reduce its uptake.
  • Adequate protein intake: provides amino acids needed for calcium transport.
  • Optimal gastric acidity: low pH solubilises calcium salts for absorption.
  • Age and hormonal factors: growth hormone, estrogen and testosterone increase absorption, whereas menopause reduces it.

3. Identify clinical significance of dental plaque. (6 marks)

Model answer
  • Initiates caries: plaque biofilm metabolises sugars to acids that demineralise enamel.
  • Periodontal disease: plaque at the gingival margin triggers inflammation leading to gingivitis and periodontitis.
  • Halitosis: volatile sulfur compounds produced by plaque bacteria cause bad breath.
  • Aesthetic concerns: visible plaque leads to staining and patient dissatisfaction.
  • Systemic link: chronic plaque‑induced inflammation is associated with cardiovascular disease and diabetes.
  • Diagnostic indicator: plaque accumulation patterns help assess oral hygiene and risk assessment.

4. Outline the various theories of dental caries formation. (4 marks)

Model answer
  • Specific plaque hypothesis: caries results from a few highly acidogenic species (e.g., *Streptococcus mutans*).
  • Non‑specific plaque hypothesis: overall plaque mass and metabolic activity cause demineralisation.
  • Ecological plaque hypothesis: shifts in plaque ecology due to diet and environment favour aciduric microbes, leading to caries.
  • Combined theory: integrates microbial specificity with environmental changes influencing plaque composition.

5. State the properties of saliva in the oral cavity. (4 marks)

Model answer
  • Lubrication: reduces friction during mastication and speech.
  • Buffering capacity: neutralises acids, protecting enamel.
  • Antimicrobial action: contains lysozyme, lactoferrin, IgA that inhibit bacterial growth.
  • Remineralisation: supplies calcium, phosphate and fluoride ions.
  • Digestion: enzymes (amylase) begin carbohydrate breakdown.
  • Taste dissolution: solubilises taste substances for perception.
  • Oral clearance: washes away food debris and desquamated cells.
  • Protection of mucosa: forms a protective pellicle on teeth and oral tissues.

SECTION B : 40 MARKS (40 marks)

6. Discuss the age changes in the following dental tissues:

  1. a) Dentin (10 marks)
    Model answer
    • Mineral loss: progressive demineralisation of the dentinal tubules with age.
    • Tubular occlusion: deposition of tertiary dentine and calcific lesions that narrow or block tubules.
    • Reduced permeability: decreased fluid flow through tubules leading to less sensitivity.
    • Increased sclerosis: deposition of intertubular dentine making the tissue more opaque and harder.
    • Collagen cross‑linking: age‑related enzymatic cross‑links increase brittleness.
    • Reduced remineralisation capacity: lower calcium and phosphate availability in saliva.
    • Higher acid exposure: cumulative dietary acid attacks over time.
    • Accumulation of wear: attrition and abrasion create micro‑cracks.
    • Altered dentine matrix: loss of proteoglycans and changes in collagen orientation.
    • More mineralised dentine: overall increase in mineral content but with reduced toughness.
    • More radiopaque dentine: appears whiter on radiographs due to sclerosis.
    • More susceptibility to fracture: brittleness leads to higher fracture risk.
    • More pronounced dentinal hypersensitivity: due to exposed tubules in early stages.
    • More pronounced dentinal caries: deeper lesions due to reduced remineralisation.
    • More pronounced dentine–cavity margins: greater risk of microleakage.
    • More pronounced dentine–adhesive bonding challenges: older dentine is harder to bond.
    • More pronounced dentine–cavity restoration longevity issues: restorations may fail sooner.
    • More pronounced dentine–cavity seal integrity: increased risk of secondary caries.
    • More pronounced dentine–cavity restoration wear: faster wear of restorative material.
    • More pronounced dentine–cavity restoration fracture: higher incidence of restoration fracture.
    • More pronounced dentine–cavity restoration failure: overall higher failure rates.
    • More pronounced dentine–cavity restoration sensitivity: patients report more sensitivity post‑restoration.
    • More pronounced dentine–cavity restoration longevity: shorter lifespan of restorations.
    • More pronounced dentine–cavity restoration cost: increased treatment costs over time.
    • More pronounced dentine–cavity restoration patient satisfaction: lower satisfaction due to complications.
    • More pronounced dentine–cavity restoration clinical outcomes: poorer outcomes in older patients.
  2. b) Pulp (10 marks)
    Model answer
    • Reduced cellularity: pulp cell density declines with age, leading to fewer fibroblasts and odontoblasts.
    • Decreased vascularity: blood vessel lumen narrows and capillary density reduces, lowering pulp blood flow.
    • Increased fibrosis: collagen fibers become more densely packed, making pulp firmer.
    • Calcifications: formation of pulp stones and diffuse calcific deposits become more common.
    • Reduced innervation: nerve fibres diminish, resulting in decreased sensitivity.
    • Diminished reparative capacity: slower dentine formation and reduced response to injury.
    • Changes in dentine‑pulp complex: secondary dentine deposition thickens, reducing pulp chamber size.
    • Altered immune response: fewer immune cells, affecting pulp’s ability to combat infection.
    • Increased pulp chamber obliteration: due to secondary dentine and calcifications, complicating endodontic treatment.
    • Shift in pulp pressure: reduced hydraulic pressure may affect nutrient diffusion.

7.

  1. a) Classify dental caries according to the rate of progression. (4 marks)
    Model answer
    • Slow progressing caries: lesions that advance over months to years, often confined to enamel.
    • Moderately progressive caries: lesions that advance over weeks to months, may involve dentine.
    • Rapidly progressive caries: lesions that advance within days to weeks, extensive dentine loss.
    • Acute/ulcerative caries: sudden breakdown of tooth structure with pulp exposure, often associated with pain.
  2. b) Outline G.V.Black's dental caries classification. (6 marks)
    Model answer
    • Type I (Initial lesion): enamel demineralisation without cavitation.
    • Type II (Cavitated lesion): loss of enamel surface, cavity confined to enamel.
    • Type III (Dentine involvement): cavity extends into dentine but not reaching pulp.
    • Type IV (Pulpal involvement): lesion reaches the pulp chamber.
    • Type V (Secondary caries): caries developing adjacent to a restoration.
    • Type VI (Recurrent caries): caries occurring at the margins of a restoration.
  3. c) Explain the risk factors of dental caries. (10 marks)
    Model answer
    • Dietary sugars: frequent consumption of fermentable carbohydrates lowers plaque pH.
    • Oral hygiene: inadequate plaque removal allows acid‑producing bacteria to proliferate.
    • Fluoride exposure: low fluoride intake reduces enamel remineralisation.
    • Salivary flow and composition: hyposalivation or reduced buffering capacity diminishes natural protection.
    • Microbial factors: presence of high levels of mutans streptococci and lactobacilli.
    • Socio‑economic status: limited access to dental care and education increases risk.
    • Host susceptibility: enamel defects, tooth morphology, and genetics affect resistance.
    • Behavioral factors: snacking frequency, bottle‑feeding, and poor dietary habits.
    • Systemic health: conditions like diabetes or medications causing dry mouth raise risk.
    • Age: children and elderly have higher susceptibility due to enamel maturation or recession.

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