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Changes in Cells & Tissues within the Oral Cavity - Coggle Diagram
Changes in Cells & Tissues within the Oral Cavity
Pathological Stimuli
Oxygen Deprivation
Hypoxia
Ischemia
↓ ATP → ion pump failure → cell swelling → necrosis
Physical Agents
Mechanical trauma
Heat / cold (burns, frostbite)
Radiation (UV, ionizing)
Electrical injury
Pressure changes
Chemical Agents & Drugs
Toxins, heavy metals
Alcohol
Therapeutic drugs
Poisons (e.g. cyanide)
Infectious Agents
Viruses
Bacteria
Fungi
Parasites
Immunologic Reactions
Autoimmune diseases
Hypersensitivity
Chronic inflammation
Genetic Abnormalities
Chromosomal defects
Gene mutations
Enzyme deficiencies
Nutritional Imbalances
Protein-calorie malnutrition
Vitamin deficiencies
Excess cholesterol / obesity
Cellular Adaptation
1. Adaptation to Intense Stimuli / Sensitive Cells
Hypertrophy
↑ cell size
↑ protein & organelle synthesis
Example: skeletal muscle hypertrophy
Hyperplasia
↑ cell number
Growth factor / hormone stimulation
Example: endometrial hyperplasia
Atrophy
↓ cell size & metabolism
↓ protein synthesis, ↑ degradation
Example: muscle atrophy after immobilization
Metaplasia
One mature cell type → another
Stem cell reprogramming
Example: squamous metaplasia in smokers
Dysplasia
Disordered cell growth & maturation
Nuclear atypia, loss of architecture
Example: cervical intraepithelial neoplasia (CIN)
2. Adaptation to Persistent Stimuli
Hypertrophy
Chronic workload
Example: cardiac hypertrophy in hypertension
Hyperplasia
Chronic stimulation
Example: liver regeneration
Atrophy
Disuse, ischemia, malnutrition
Example: denervation atrophy
Metaplasia
Chronic irritation
Protective but ↑ cancer risk
3. Adaptation Affecting Growth & Differentiation
Hypertrophy
↑ functional demand
Example: left ventricular hypertrophy
Hyperplasia
Physiologic (breast during pregnancy)
Pathologic (endometrial hyperplasia)
Metaplasia
Reversible change
Long-term risk → dysplasia, cancer
Cell Injury & Cell Death
1. Apoptosis (Programmed Cell Death)
Purpose
Remove damaged / unnecessary cells
No inflammation
Intrinsic (Mitochondrial) Pathway
DNA damage, hypoxia, oxidative stress
BAX/BAK ↑ → cytochrome c release
Extrinsic (Death Receptor) Pathway
Fas, TNF receptors
Caspase-8 activation
Final Common Pathway
Caspase-3, 6, 7 activation
Apoptotic bodies → phagocytosis
Oral relevance
Epithelial turnover
Periodontal disease
Cancer therapy response
2. Reversible Cell Injury
Cell swelling (hydropic change)
Membrane blebbing
Mild mitochondrial swelling
ER dilation, ribosome detachment
Chromatin clumping
Example
Mild hypoxia in oral epithelium
3. Irreversible Cell Injury (Necrosis)
Permanent mitochondrial damage
Membrane rupture
Calcium influx → enzyme activation
Nuclear changes
Pyknosis
Karyorrhexis
Karyolysis
Types of necrosis
Coagulative
Liquefactive
Caseous
Fat
Oral examples
Pulp necrosis
Oral abscess
Chemical burns of mucosa
Requirements for Normal Tissue Function
Adequate oxygen & nutrients
Normal blood circulation
Intact cell membranes & DNA
Balanced ions (Na⁺, K⁺, Ca²⁺)
Adequate ATP production
Proper ECM support
Balanced proliferation & apoptosis
Effective repair & immune balance
Apoptosis vs Necrosis
Apoptosis
Programmed
ATP-dependent
Cell shrinkage
No inflammation
Necrosis
Accidental
ATP depletion
Cell swelling
Inflammation present
Disorders Related to Fluids, Electrolytes & Blood
Fluids & Electrolytes
Edema
Hyperkalemia
Dehydration
Blood
Anemia
Bleeding diathesis
Hypertension
Cardiomyopathy
Calcium Imbalance in Oral Cavity
Hypocalcemia
Delayed tooth eruption
Enamel defects
Hypercalcemia
Loose teeth
Reduced jaw bone density
Oral tori
Role of calcium
Enamel strength
Periodontal support
Prevention of tooth loss
Oral Pigmentation
Endogenous
Melanin pigmentation (physiologic)
Oral melanoma (pathologic)
Exogenous
Amalgam tattoo
Drug-induced pigmentation