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Changes in Cells and Tissues in Oral Cavity, Medinna Rasha - 2506557816 -…
Changes in Cells and Tissues in Oral Cavity
Pathological stimuli causing cellular & tissue changes
Hypoxia / Ischemia
↓ oxygen delivery → ↓ ATP
Causes: ischemia, anemia, CO poisoning, blood loss
Physical agents
Trauma, heat, cold, radiation, electricity
DNA damage, membrane rupture
Chemical agents & drugs
Poisons, alcohol, pollutants, medications
Enzyme inhibition, membrane injury
Infectious agents
Bacteria, viruses, fungi, parasites
Toxins, immune-mediated injury, invasion
Immunologic reactions
Autoimmune disease, hypersensitivity
Chronic inflammation → tissue damage
Genetic abnormalities
Mutations, chromosomal defects
Abnormal proteins, cell cycle dysregulation
Nutritional imbalances
Deficiency (vitamins, protein)
Excess (obesity)
Cellular adaptation to intense stimuli / sensitive cells
Hypertrophy
↑ cell size
Mechanism: ↑ protein & organelle synthesis
Examples
Cardiac hypertrophy (hypertension)
Skeletal muscle (exercise)
Hyperplasia
↑ cell number
Mechanism: growth factor–stimulated proliferation
Examples
Breast glands (pregnancy)
Liver regeneration
Bone marrow after blood loss
Atrophy
↓ cell size & function
Mechanism
↓ protein synthesis
↑ ubiquitin–proteasome degradation
Autophagy
Examples
Immobilized muscle
Brain ischemia in elderly
Metaplasia
Replacement of one mature cell type by another
Mechanism: stem cell reprogramming
Examples
Squamous metaplasia (smokers)
Salivary duct obstruction
Cellular adaptation to persistent (chronic) stimuli
Chronic stress → long-term adaptation
Hypertrophy
Chronic increased workload
Example: LV hypertrophy (hypertension)
Hyperplasia
Sustained hormonal/growth factor stimulation
Examples
Endometrial hyperplasia (estrogen excess)
Compensatory liver hyperplasia
Atrophy
Reduced demand or nutrition
Mechanism: proteasome + autophagy
Examples
Muscle disuse
Aging brain
Metaplasia
Chronic irritation
Examples
Bronchial squamous metaplasia
Barrett esophagus
Adaptation to stimuli altering cell growth & differentiation
Hyperplasia
Physiologic
Hormonal (breast at puberty/pregnancy)
Compensatory (liver after hepatectomy)
Pathologic
Excess hormonal stimulation
Example: endometrial hyperplasia
Metaplasia
Change in differentiation pattern
Stem cell reprogramming
Example
Squamous metaplasia in smokers
Apoptosis due to mitochondrial damage (intrinsic pathway)
Initiation
DNA damage, oxidative stress, ↓ growth factors
Bcl-2 family activation
Pro-apoptotic: Bax, Bak
Mitochondrial outer membrane permeabilization (MOMP)
Pore formation in mitochondrial membrane
Cytochrome c release
Apoptosome formation
Cytochrome c + Apaf-1 + ATP
Caspase activation
Caspase-9 → caspase-3,-6,-7
Outcome
DNA fragmentation
Cell shrinkage
Apoptotic bodies
Reversible vs irreversible cell injury (necrosis)
A. Reversible cell injury
Mechanisms
Mild ATP depletion
Na⁺/K⁺ pump failure → cell swelling
Anaerobic glycolysis → lactic acidosis
Ribosome detachment → ↓ protein synthesis
Mild mitochondrial swelling
Morphology
Hydropic change
Fatty change
Examples
Transient ischemia
Early alcohol-induced fatty liver
B. Irreversible injury (necrosis)
Mechanisms
Severe mitochondrial damage
Massive Ca²⁺ influx
Membrane rupture
Lysosomal enzyme release
Oxidative stress
Nuclear changes
Pyknosis → karyorrhexis → karyolysis
Examples
MI → coagulative necrosis
Brain infarct → liquefactive necrosis
Burns, toxins, pancreatitis
Mechanisms of apoptosis
Definition
Programmed, energy-dependent cell death
Key features
Cell shrinkage
Chromatin condensation
Membrane blebbing
Apoptotic bodies
No inflammation
Caspases
Initiator: caspase-8,-9
Executioner: caspase-3,-6,-7
Pathways
Intrinsic: mitochondrial, cytochrome c
Extrinsic: death receptors (Fas, TNF)
Outcome
Rapid phagocytosis
Tissue homeostasis
Differences between apoptosis and necrosis
Apoptosis
Programmed, regulated
ATP-dependent
Cell shrinkage
No inflammation
Caspase-mediated
Necrosis
Accidental, uncontrolled
ATP depletion
Cell swelling & rupture
Inflammation present
Enzyme leakage
Requirements for normal tissue function
Adequate oxygen
Sufficient nutrients
Effective blood circulation
Intact cell membranes
Normal mitochondrial ATP production
Proper enzymatic activity
Efficient waste removal
Balanced hormones & neural control
Normal immune defense
Stable internal environment (pH, temp, electrolytes)
Disorders from fluid, electrolyte & blood disturbances
Hemodynamic disorders
Edema
↑ hydrostatic pressure
↓ oncotic pressure
Lymph obstruction
Hyperemia
Active ↑ blood flow
Example: inflamed gingiva
Congestion
Passive venous stasis
Electrolyte disorders
Na⁺ imbalance → CNS symptoms
K⁺ imbalance → arrhythmias
Ca²⁺ imbalance
Acid–base disorders
Blood disorders
Anemia → pale oral mucosa
Polycythemia → reddish hue
Thrombocytopenia → gingival bleeding
Oral disorders due to calcium imbalance
Hypocalcemia
↓ enamel mineralization
Oral manifestations
Enamel hypoplasia
Delayed eruption
↑ caries
Paresthesia, muscle spasms
Example
Vitamin D deficiency
Hypercalcemia
Altered bone remodeling
Oral findings
Loss of lamina dura
Jaw bone resorption
Tooth mobility
Example
Hyperparathyroidism
Oral pigmentation
Melanin-based
Physiologic
Racial pigmentation
Gingiva, buccal mucosa
Pathologic
Melanotic macule
Melanoacanthoma
Systemic
Addison disease
Peutz–Jeghers syndrome
Neoplastic
Oral melanoma
Non-melanin
Hemoglobin-based
Erythema, vascular lesions
Exogenous
Amalgam tattoo
Drug-induced (minocycline)
Medinna Rasha - 2506557816