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PATHOLOGY NOTES - BDS (Manipal Academy)

References: Essential Pathology for Dental Students (Harsh Mohan, 3rd ed.) | General & Systemic Pathology (Underwood & Cross, 7th ed.) | Robbins Basic Pathology

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SECTION 1: INTRODUCTION TO PATHOLOGY & BASIC TERMINOLOGIES

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1. What is Pathology?

• Gross or microscopic appearance (morphology) of cells and tissues
• Genes and proteins
• Biochemical alterations in body fluids (blood, urine)

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2. Relevance of Pathology

• Pathology bridges basic sciences and clinical medicine
• It explains why a patient is sick and how the disease progressed
• It guides rational treatment - e.g., identifying mutations in cancer has led to precision (personalized) medicine where therapies are tailored to individual patients
• Diseases presenting with similar features (e.g., cancers of the same organ) may show important molecular differences (mutations, epigenetic changes) that determine treatment

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3. Basic Terminologies

a. Aetiology (Etiology)

b. Pathogenesis

• Etiology = why a disease arises
• Pathogenesis = how a disease develops
• Both are essential for understanding disease and developing rational treatments.

c. Pathological and Clinical Manifestations

• Pathological manifestations: Structural changes in cells and tissues observed grossly (naked eye) or microscopically (histology, cytology)
• Clinical manifestations: Signs and symptoms experienced by the patient or detected on examination (e.g., fever, pain, swelling, jaundice)

d. Complications & Sequelae

• Complications: Additional diseases or problems that arise as a consequence of the primary disease (e.g., sepsis as a complication of pneumonia)
• Sequelae (singular: sequela): Conditions that follow and are caused by a disease after it has resolved (e.g., scarring after myocardial infarction; limb paralysis after stroke)

e. Prognosis

f. Syndrome

g. Lesion

• Gross (visible to naked eye): ulcer, tumor mass
• Microscopic: cellular change seen on histology

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4. Branches of Pathology and Their Scope

a. Histopathology

• Study of tissue sections under the microscope (light microscopy, electron microscopy)
• Tissues are fixed (usually in formalin), processed, embedded in paraffin, sectioned, and stained (H&E = Haematoxylin and Eosin)
• Used for: Biopsy diagnosis of tumors, inflammatory diseases, infections
• Scope in dentistry: Oral biopsies, salivary gland tumors, periodontal tissues

b. Cytopathology

• Study of individual cells (not tissue architecture) for disease diagnosis
• Methods: Fine Needle Aspiration Cytology (FNAC), exfoliative cytology (Pap smear), sputum cytology, oral scraping
• Advantages: Minimally invasive, quick, inexpensive
• Scope in dentistry: Oral cancer screening, FNAC of lymph nodes and salivary gland swellings

c. Haematology

• Study of blood and blood-forming organs (bone marrow, spleen, lymph nodes)
• Includes: Complete blood count (CBC), peripheral blood smear examination, bone marrow biopsy
• Scope in dentistry: Pre-operative bleeding/clotting assessment, diagnosis of anaemia, leukemia (which can present with oral manifestations)

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SECTION 2: CELL INJURY & ADAPTATION

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CELL ADAPTATION

Definition of Cell Growth, Differentiation, and Adaptation

• Cell growth: Increase in cell size (hypertrophy) or cell number (hyperplasia)
• Cell differentiation: Process by which precursor (stem) cells become specialized cell types with specific structure and function
• Cell adaptation: The ability of cells to adjust their structure and function in response to physiologic stress or injurious stimuli to achieve a new steady state while preserving viability. This maintains homeostasis.

Key concept: Cells actively interact with their environment. When stressed, they can adapt (achieving a new steady state), or if the stress exceeds adaptive capacity, they undergo injury and death. - Robbins Basic Pathology

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Types of Cell Adaptations

a. Hypertrophy

• Definition: Increase in the size of cells, resulting in increased size of the organ. No new cells are produced.
• Occurs in cells that cannot divide (e.g., cardiac muscle, skeletal muscle, neurons)
• Mechanism: Increased synthesis of structural proteins; activation of growth factors; gene expression changes (e.g., shift from alpha to beta myosin heavy chain in cardiac hypertrophy - produces slower but more energy-efficient contractions)

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b. Hyperplasia

• Definition: Increase in the number of cells in an organ due to increased cell proliferation. Can occur alongside hypertrophy, in response to same stimuli.
• Occurs only in tissues with cells capable of replication (e.g., liver, epithelium, glands - NOT cardiac muscle or neurons)

Note: Hyperplasia is controlled - cells respond to normal growth signals. If growth becomes autonomous, it can lead to cancer.

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c. Atrophy

• Definition: Decrease in the size of cells (and thus the organ), caused by loss of cell substance. Different from aplasia (failure of development) or hypoplasia.
• Mechanism: Decreased protein synthesis + increased protein degradation (via ubiquitin-proteasome pathway and autophagy)

Atrophy involves a balance between synthesis and degradation shifting toward degradation. The mechanism includes autophagy - cells digest their own organelles for survival. Atrophied cells may not be dead but have reduced function.

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d. Metaplasia

• Definition: A reversible change in which one differentiated cell type is replaced by another differentiated cell type (adult cell type substitution).
• Represents a reprogramming of stem cells in response to chronic stress
• The new cell type is better suited to survive the adverse environment

If the stimulus causing metaplasia persists, it can progress to dysplasia and eventually to malignant transformation (cancer). Metaplasia itself is not cancerous but represents increased risk.

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e. Dysplasia

• Definition: Disordered cellular growth with loss of uniformity of individual cells and loss of architectural orientation. Not strictly an adaptive response - it is a pre-malignant change.
• Features: Pleomorphism (variation in cell size/shape), nuclear enlargement and hyperchromasia, increased mitotic figures, loss of normal tissue architecture

• Often seen in epithelial surfaces (oral, cervical, bronchial)
• Graded as mild, moderate, or severe
• Severe dysplasia is essentially carcinoma in situ
• Can potentially regress if stimulus is removed (mild dysplasia), but severe dysplasia often progresses to invasive cancer

Dysplasia is a crucial concept in oral pathology - oral epithelial dysplasia in leukoplakia/erythroplakia is a key marker of malignant potential in dental practice.

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NECROSIS

Definition

• Breakdown of cellular membranes
• Leakage and enzymatic digestion of cellular contents
• An accompanying inflammatory reaction in the host tissue

• Pyknosis: Nuclear shrinkage with increased basophilia (DNA condenses into a dark, shrunken mass)
• Karyorrhexis: Fragmentation of the pyknotic nucleus
• Karyolysis: Fading of basophilia due to DNase-mediated digestion of DNA; nucleus dissolves in 1-2 days

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Types of Necrosis (with Clinical Examples)

a. Coagulative Necrosis

• Mechanism: Tissue architecture is preserved for days after injury because the injury denatures both structural proteins AND enzymes, limiting proteolysis (self-digestion)
• Appearance: Firm texture; eosinophilic, anucleate "ghost cells" (cell outlines preserved but nuclei gone)
• Cause: Ischemia (blocked blood supply)
• Location: All solid organs EXCEPT the brain
• Clinical example: Myocardial infarction (heart attack) - area of coagulative necrosis in heart. Also: renal infarct, splenic infarct
• Dental relevance: Bone infarction, dry socket (alveolar osteitis)

b. Liquefactive (Colliquative) Necrosis

• Mechanism: Dead cells are completely digested by leukocyte enzymes or the cell's own enzymes, transforming tissue into a viscous liquid
• Appearance: Soft, creamy-yellow pus (in infections); fluid-filled cavity
• Causes:
  • Bacterial or fungal infections (leukocytes accumulate and release hydrolytic enzymes)
  • Hypoxic death in the brain (CNS specifically undergoes liquefactive, not coagulative necrosis - for unclear reasons)
• Clinical examples: Brain abscess, cerebral infarction; dental abscess (dental pus is liquefactive necrosis)

c. Caseous Necrosis

• Mechanism: A combination of coagulative and liquefactive necrosis; complete tissue architecture is lost (unlike coagulative)
• Appearance: Gross: Soft, friable, white-cheese like material (hence "caseous" = cheese-like). Microscopic: Amorphous, granular, eosinophilic debris without cell outlines, surrounded by a granulomatous inflammation (epithelioid macrophages, Langhans giant cells, lymphocytes)
• Cause: Almost always tuberculosis (Mycobacterium tuberculosis); also other mycobacteria, fungi
• Clinical example: Caseous center of a tuberculous lymph node (scrofula); pulmonary TB cavity
• Dental relevance: Cervical lymph node tuberculosis; orofacial TB

d. Fibrinoid Necrosis

• Mechanism: Deposition of fibrin-like material in vessel walls due to immune complex deposition and complement activation, causing necrosis of vessel wall
• Detection: Only by microscopic examination (not grossly visible)
• Appearance: Bright pink, homogeneous, smudgy deposits in vessel walls on H&E staining
• Causes: Immune complex diseases (e.g., vasculitis); malignant hypertension; autoimmune diseases (rheumatoid arthritis, systemic lupus erythematosus)
• Clinical example: Blood vessel walls in malignant hypertension; polyarteritis nodosa

e. Fat Necrosis

• Mechanism: Destruction of fat cells by lipases, which release fatty acids that combine with calcium to form calcium soaps (saponification)
• Two forms:
  1. Enzymatic fat necrosis: Seen in acute pancreatitis - pancreatic lipases escape and digest peripancreatic fat and omentum
  2. Traumatic fat necrosis: Blunt trauma to fat-rich areas (e.g., breast)
• Appearance: Chalky white deposits (calcium soap); gritty texture
• Clinical example: Peripancreatic fat necrosis in acute pancreatitis; breast fat necrosis after trauma or surgery

f. Gangrene

• Definition: Large area of necrosis (usually of a limb or part) with superimposed bacterial infection and putrefaction
• Types:

Clinically important: Dry gangrene is relatively safe with slow progression; wet gangrene is a surgical emergency. Gas gangrene is life-threatening.

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QUICK SUMMARY TABLE

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