National Board Dental Examination / Integrated National Board Dental Examination (INBDE) General and Oral Pathology Syllabus

General and Oral Pathology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for General and Oral Pathology in National Board Dental Examination / Integrated National Board Dental Examination (INBDE), not a summary of it.

1. 1

   General Pathology Mechanisms

   5 topics

   • Cell injury, adaptation, and necrosis
     • Reversible versus irreversible injury
     • Atrophy, hypertrophy, hyperplasia, metaplasia
   • Acute and chronic inflammation
     • Vascular and cellular events
     • Mediators and chemotaxis
   • Tissue repair, regeneration, and wound healing
   • Neoplasia principles and tumor biology
     • Benign versus malignant characteristics
     • Carcinogenesis and metastatic spread
   • Hemodynamic disorders and thrombosis
2. 2

   Immunology and Immune-Mediated Disease

   3 topics

   • Innate and adaptive immunity
     • Cells and mediators of immune response
     • Antigen presentation and antibody function
   • Hypersensitivity reactions types I-IV
   • Autoimmune and immunodeficiency disorders
     • Sjogren syndrome and lupus oral findings
     • HIV/AIDS oral manifestations
3. 3

   Diseases of Hard Dental Tissues

   4 topics

   • Dental caries pathogenesis and progression
   • Developmental anomalies of teeth
     • Number, size, and shape anomalies
     • Enamel and dentin structural defects
   • Pulpal and periapical pathology
     • Reversible and irreversible pulpitis
     • Periapical granuloma, cyst, and abscess
   • Tooth wear: attrition, abrasion, erosion, abfraction
4. 4

   Oral Soft Tissue and Bone Pathology

   5 topics

   • Odontogenic and non-odontogenic cysts
     • Radicular, dentigerous, and odontogenic keratocyst
   • Odontogenic tumors and fibro-osseous lesions
     • Ameloblastoma and odontoma
     • Fibrous dysplasia and ossifying fibroma
   • Premalignant lesions and oral squamous cell carcinoma
     • Leukoplakia and erythroplakia
     • Risk factors and clinical staging
   • Vesiculobullous and ulcerative mucosal conditions
     • Aphthous ulcers, lichen planus, pemphigus
   • Salivary gland disorders and tumors

General and Oral Pathology flashcards for National Board Dental Examination / Integrated National Board Dental Examination (INBDE)

20 of 58 cards from the General and Oral Pathology deck — real questions with worked answers.

1. What are the two principal ultrastructural hallmarks of reversible cell injury seen under the microscope?

   Cellular swelling (hydropic change from failed Na+/K+ ATPase) and fatty change (steatosis). Both lack membrane rupture, so they are reversible if the stimulus is removed.

2. List the four major cellular adaptations to stress and give a one-word change for each.

   Hyperplasia (increased cell number), hypertrophy (increased cell size), atrophy (decreased size/number), and metaplasia (change of one mature cell type to another).

3. How do necrosis and apoptosis differ in membrane integrity, inflammation, and energy requirement?

   Necrosis: membrane disrupted, elicits inflammation, ATP-independent (passive). Apoptosis: membrane intact (forms apoptotic bodies), no inflammation, ATP-dependent (active, programmed).

4. Match each tissue/disease to its characteristic type of necrosis: heart, brain, tuberculosis, acute pancreatitis.

   Heart (ischemia) = coagulative; brain (ischemia) = liquefactive; tuberculosis = caseous; acute pancreatitis = fat necrosis.

5. What is the central biochemical event that makes ischemic/hypoxic injury reversible versus irreversible?

   Loss of mitochondrial ATP is reversible; once severe membrane damage and massive Ca2+ influx occur (activating enzymes and causing mitochondrial permeability transition), injury becomes irreversible.

6. Name the five cardinal signs of acute inflammation and the Latin terms.

   Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).

7. Which cell is the predominant leukocyte in acute inflammation versus chronic inflammation?

   Acute inflammation: neutrophils (PMNs). Chronic inflammation: macrophages, lymphocytes, and plasma cells.

8. List the ordered steps of leukocyte extravasation and the key adhesion molecules at each step.

   Margination/rolling (selectins–sialyl Lewis X), firm adhesion (integrins–ICAM-1/VCAM-1), transmigration/diapedesis (PECAM-1/CD31), then chemotaxis toward the stimulus.

9. What are the chemical mediators responsible for vasodilation, increased vascular permeability, pain, and fever in inflammation?

   Vasodilation: histamine, prostaglandins, NO. Permeability: histamine, leukotrienes C4/D4/E4, bradykinin. Pain: bradykinin, PGE2. Fever: IL-1, IL-6, TNF, prostaglandins.

10. What defines a granuloma, and name the two main types with examples.

    A granuloma is a focal collection of activated (epithelioid) macrophages often with multinucleated giant cells. Caseating (TB, fungal) and non-caseating (sarcoidosis, Crohn, foreign body).

11. Contrast healing by regeneration versus repair by fibrosis (scar).

    Regeneration restores normal tissue using residual cells (requires labile/stable cells and intact stroma). Repair by connective tissue (scar) occurs when tissue is non-regenerative or the framework is destroyed.

12. What are the components and timing of granulation tissue formation in wound healing?

    Granulation tissue (proliferating fibroblasts + new capillaries/angiogenesis + loose ECM) appears around days 3–5, giving a soft pink, granular appearance before maturation into scar.

13. Differentiate healing by primary versus secondary intention.

    Primary intention: clean, approximated wound edges (e.g., sutured surgical incision), minimal tissue loss, small scar. Secondary intention: large tissue gap, more granulation tissue, wound contraction by myofibroblasts, larger scar.

14. Which vitamin and which mineral are essential cofactors for collagen synthesis/cross-linking in wound healing?

    Vitamin C (cofactor for prolyl/lysyl hydroxylase in collagen cross-linking) and zinc (cofactor for collagenase/metalloproteinases in remodeling).

15. Define neoplasia and distinguish the suffixes -oma, -carcinoma, and -sarcoma.

    Neoplasia is autonomous, unregulated clonal cell growth. -oma usually denotes a benign tumor; carcinoma is a malignant epithelial tumor; sarcoma is a malignant mesenchymal (connective tissue) tumor.

16. List the key features that distinguish a malignant from a benign tumor.

    Malignant: poorly differentiated/anaplastic, rapid growth, infiltrative/invasive, high mitoses, metastasis, poorly demarcated. Benign: well differentiated, slow, encapsulated/non-invasive, no metastasis.

17. What is the difference between a proto-oncogene, an oncogene, and a tumor suppressor gene?

    A proto-oncogene normally promotes growth; mutation makes it a constitutively active oncogene (gain of function, dominant). Tumor suppressors normally inhibit growth; both alleles must be lost (loss of function, recessive — two-hit hypothesis).

18. Name the three main routes of metastatic spread and the typical tumor type favoring each.

    Lymphatic spread (carcinomas), hematogenous spread (sarcomas), and seeding of body cavities (e.g., ovarian carcinoma in peritoneum).

19. What are the six classic hallmarks of cancer described by Hanahan and Weinberg?

    Self-sufficiency in growth signals, insensitivity to anti-growth signals, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion/metastasis.

20. State Virchow's triad of factors predisposing to thrombosis.

    Endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability.

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