Oral Biology II: Main Exam, 24 March 2026
Mount Kenya University · Department of Dental Sciences · Diploma in Community Oral Health · DDS2212
Oral Biology II (DDS2212) Mount Kenya University 2025-2026 past exam with model answers covering calcium functions, tooth mineralization, enamel ageing, fluoride use, deg
Instructions: ATTEMPT ALL QUESTIONS IN SECTION A AND ANY OTHER TWO (2) IN SECTION B
SECTION A
1. Explain FOUR (4) the functions of calcium in the body. (8 marks)
- Structural role: Calcium is a major component of hydroxyapatite, providing hardness and strength to bone and teeth.
- Muscle contraction: Calcium ions trigger interaction between actin and myosin filaments, enabling skeletal, cardiac and smooth muscle contraction.
- Nerve transmission: Calcium influx at synaptic terminals facilitates release of neurotransmitters.
- Blood clotting: Calcium acts as a co‑factor for several steps in the coagulation cascade, essential for fibrin formation.
2. Identify factors influencing mineralization of teeth. (4 marks)
- Genetic factors – inherited enamel and dentin composition.
- Systemic health – nutritional status (vitamin D, calcium), endocrine disorders, chronic diseases.
- Local oral environment – pH, saliva flow and composition.
- Fluoride exposure – adequate fluoride enhances mineral deposition; deficiency impairs it.
3. Outline FIVE (5) age changes in the enamel. (5 marks)
- Surface wear – gradual loss of outer enamel due to attrition and erosion.
- Increased translucency – enamel becomes more translucent with age as mineral density changes.
- Reduced thickness – secondary dentin deposition narrows the enamel layer.
- Color change – yellowing occurs as underlying dentin shows through.
- Decreased permeability – older enamel is less porous, reducing diffusion of fluids.
4. Explain uses of Fluoride in dentistry. (4 marks)
- Caries prevention – low‑dose fluoride promotes remineralisation and inhibits demineralisation of enamel.
- Reduction of bacterial activity – fluoride interferes with bacterial metabolism and acid production.
- Strengthening of enamel – incorporation of fluoride into hydroxyapatite forms fluorapatite, which is more acid‑resistant.
- Therapeutic use – topical applications (gel, varnish) and systemic supplementation (water, tablets) for high‑risk patients.
5. Describe THREE (3) phases of deglutition. (9 marks)
- Oral preparatory phase – food is chewed, mixed with saliva, and formed into a bolus; tongue positions the bolus against the hard palate.
- Pharyngeal phase – the soft palate elevates, the epiglottis closes, and the bolus is propelled through the pharynx by sequential contraction of pharyngeal muscles.
- Esophageal phase – peristaltic waves of the esophagus move the bolus toward the stomach.
- Key actions: (i) closure of the nasopharynx, (ii) protection of the airway, (iii) coordinated muscle contractions.
SECTION B
1. Discuss chemical composition of teeth. (20 marks)
- Enamel – ~96% hydroxyapatite (crystalline calcium‑phosphate), 1–2% water, <1% organic matrix (amelogenins, enamelins).
- Dentin – ~70% hydroxyapatite, 20% organic matrix (type I collagen, dentin phosphoproteins), 10% water.
- Cementum – ~45–50% hydroxyapatite, 30% organic collagen, 20% water; contains cementoblasts.
- Pulpal dentin – similar to dentin but with higher water content (~30%) and cellular elements (odontoblasts, fibroblasts).
- Periodontal ligament – collagen fibres (type I) with embedded fibroblasts, small amounts of calcium‑phosphate crystals.
- Mineral ions – calcium, phosphate, fluoride (trace) incorporated into hydroxyapatite crystals.
- Organic proteins – amelogenin (enamel), collagen (dentin, cementum), non‑collagenous proteins (DSPP, osteocalcin).
- Water – present in all tissues, influencing permeability and ion exchange.
- Trace elements – magnesium, sodium, potassium, carbonate that modify crystal size and solubility.
- Structural hierarchy – enamel rods, dentinal tubules, cementum layers, each with distinct composition contributing to overall tooth function.
2. Explain hormones which have influence on soft and hard tissues of oral cavity. (20 marks)
- Sex hormones – Estrogen promotes gingival collagen synthesis and bone density; deficiency leads to increased periodontal breakdown.
- Progesterone – Increases vascular permeability and gingival inflammation; enhances plaque‑induced gingivitis.
- Testosterone – Supports alveolar bone maintenance; low levels associated with bone loss.
- Parathyroid hormone (PTH) – Regulates calcium homeostasis; excess causes alveolar bone resorption, deficiency impairs bone formation.
- Calcitonin – Lowers serum calcium, inhibiting osteoclast activity and protecting alveolar bone.
- Growth hormone (GH) / IGF‑1 – Stimulates proliferation of periodontal ligament fibroblasts and osteoblasts, aiding tissue repair.
- Thyroid hormones (T3/T4) – Essential for normal development of dentin and enamel; hypothyroidism delays tooth eruption and reduces bone turnover.
- Cortisol (glucocorticoids) – Anti‑inflammatory but chronic excess suppresses fibroblast activity and reduces collagen, weakening gingiva.
- Vitamin D (calcitriol) – Hormonal form enhances calcium absorption and osteoblast function, crucial for alveolar bone mineralisation.
- Insulin – Anabolic effects on periodontal fibroblasts; uncontrolled diabetes impairs wound healing and increases bone loss.
- Melatonin – Modulates oxidative stress in gingival tissues and may influence bone remodeling.
- Prostaglandins (e.g., PGE2) – Though not classic hormones, act locally to mediate inflammation and bone resorption in periodontitis.
- Adrenaline/Noradrenaline – Stress‑induced vasoconstriction can reduce gingival blood flow, affecting tissue health.
- Leptin – Links adipose tissue to bone metabolism; elevated levels may affect periodontal inflammation.
- Erythropoietin – Stimulates angiogenesis in periodontal tissues, supporting healing.
- Oxytocin – Emerging evidence of role in bone formation and periodontal regeneration.
- Serotonin – Influences bone density through central pathways; altered levels can affect alveolar bone.
- Renin‑angiotensin system components – Angiotensin II promotes inflammation and bone resorption in periodontium.
- Fibroblast growth factors (FGFs) – Promote proliferation of oral mucosal cells and odontoblast differentiation.
- Bone morphogenetic proteins (BMPs) – Critical for dentin and alveolar bone formation and repair.
3. Discuss different types of oral defense mechanisms in the oral cavity. (20 marks)
- Mechanical barrier – Keratinised stratified squamous epithelium and tight junctions prevent microbial invasion.
- Salivary flow – Flushes debris, dilutes acids, and provides antimicrobial proteins (lysozyme, lactoferrin, peroxidases).
- Oral microbiome – Commensal bacteria occupy niches, produce bacteriocins and compete with pathogens.
- Innate immune cells – Neutrophils migrate rapidly into gingival crevice; macrophages phagocytose microbes.
- Antimicrobial peptides – Defensins, cathelicidins, histatins directly kill bacteria and fungi.
- Immunoglobulins – Secretory IgA neutralises antigens and prevents adherence to mucosal surfaces.
- Complement system – Opsonises pathogens and triggers inflammation for clearance.
- Mucosal immunity – Langerhans cells present antigens to T‑cells, initiating adaptive responses.
- Cytokine network – IL‑1, IL‑6, TNF‑α coordinate inflammation and tissue repair.
- Bone remodeling regulation – RANKL/OPG balance controls alveolar bone turnover, limiting pathogen‑induced resorption.
- Salivary buffering capacity – Bicarbonate neutralises acids, protecting enamel and limiting bacterial growth.
- pH‑dependent enzyme activity – Salivary amylase and lysozyme function optimally at neutral pH, aiding defence.
- Mucosal shedding – Desquamation removes attached microbes.
- Oral mucosal mucus layer – Traps microbes and contains glycoproteins with antimicrobial activity.
- Taste buds and sensory nerves – Detect irritants, triggering reflexes (salivation, swallowing) that clear pathogens.
- Systemic immunity link – Circulating antibodies and cells can migrate to periodontal tissues during infection.
- Healing mechanisms – Growth factors (EGF, TGF‑β) promote epithelial restitution after injury.
- Microbial antagonism – Production of hydrogen peroxide and organic acids by commensals suppresses pathogens.
- Behavioral factors – Chewing stimulates saliva; oral hygiene practices mechanically remove biofilm.
- More answers: Genetic polymorphisms influencing immune response, nutritional status (vitamins A, C, D), and hormonal influences (e.g., estrogen) also modulate oral defence.