Solitary/multiple subtypes
Etiology:
Clinical:
Etiology: Injury to peripheral nerve Eg. XLA + disturbance in regeneration process
Clinical: Tenderness – severe pain
Histology: Bundles of nerves in haphazard/tortuous arrangement + collagenous tissue
Management: Surgical resection
Not metastasize, but locally invasive
Common site: Mandible > Maxilla
Clinical:
Radiology:
Histology:
Management:
Epidemiology: Females 4th decade
Histology: Dispersed stellate/spindle shaped fibroblasts in loose myxoid stroma
Clinical:
Management:
Types:
Soft elastic yellow color swelling in cheek/tongue
Histology:
Fat cells histologically similar to normal fat cells but metabolically different as fat not lost from lipoma on starvation
Clinical:
Site:
Diagnosis:
Management:
Histology: Adipocytes in fibrous locules
Reactive hyperplastic mass – occurs on gingiva
Origin: CT
Epidemiology: Young adults, F>M
Clinical: Pedunculated/sessile mass, color of surrounding tissues
Histology:
Management:
1. Tumors of fibrous tissues – Peripheral fibroma
2. Tumors of adipose/CT:
3. Developmental tumor – Facial teratoma
4. Tumors of vascular tissue
5. Tumors of neural tissues:
Neoplasm:
The following are pathological growths but not neoplasms:
Teratoma:
Choristoma: Ectopic rest of normal tissue
Hamartoma: Disorganized + mature differentiated cells of a different site eg. Hemangioma
The following may occur physiologically:
Hyperplasia:
Hypertrophy: Increased size of cell eg. muscular hypertrophy
a) Direct acting compounds
b)Indirect acting compounds (procarcinogens)
c) Promoters
a) Ultraviolet rays – Formation of pyrimidine dimers due to UVB (280-320nm) damage
b) Ionizing radiation
a) DNA viruses
b) RNA viruses
c) Helicobacter pylori – Uncontrolled proliferation, particularly of B cells in response to chronic infection – causes gastric carcinoma
d) Endoparasites – Schistosoma spp.
| Diagnostics | Benign tumor | Malignant tumor |
| Clinical features | ||
| Growth rate | Slow | Rapid |
| Ulceration | – | ✓ |
| Indentation | – | ✓ |
| Metastases | – | ✓ |
| Paraneoplastic syndromes | – | ✓ |
| Radiographic features | ||
| Peripheral demarcation | Well demarcated | Poorly demarcated |
| Expansile masses | ✓ | – |
| Floating teeth osteolysis | – | ✓ |
| Histopathological features | ||
| Hyperchromatic nuclei | – | ✓ |
| Invasiveness | – | ✓ |
| Mitotic index | Low | High |
| Abnormal Ag secretion | Rare | Present |
| Nuclear-cytoplasmic ratio | Normal | Increased |
| Desmosomal contact | ✓ | – |
| Apoptotic bodies | Normal | Increased |
| Loss of cell polarity | – | ✓ |
| Aneuploidy | – | ✓ |
| Polymorphic nuclei | – | ✓ |
| Prominent nucleoli | – | ✓ |
| Cellular differentiation | Mature cells | Immature cells |
| Cellular pleomorphism | – | ✓ |
1. Multistep process – acquisition of genotypic changes – results in phenotypic attributes – necessary for tumor progression
2. These changes induced in a cell by – mutations in genes of DNA – and are non lethal genetic damage
3. Mutations are hereditary or environmental (chemical, virus, radiation)
4. Modes of mutation:
5. Damaged progenitor cells proliferate in clonal manner – therefore excessive growth and local invasiveness – promote tumor progression
6. Principle targets of genetic cell damage:
a) Proto-oncogenes:
b) Anti-oncogenes/ tumor suppressor genes:
c) Apoptosis regulatory genes:
d) DNA repair genes:
e) Decreased telomerase activity:
Factors that contribute to these are:
Angiogenic cytokines:
Step wise acquisition of mutations to produce phenotypes that:
| Environmental factors → | DNA damage → | Genotypic change → | Phenotypic change → | Malignancy |
| Virus, tobacco, genetic, UVB, alcohol, malnutrition | 1. Direct 2. Chronic oxidative stress (ROS) | 1. Cell growth + 2. Neoangiogenesis + 3. Immune evasion + 4. Metastasis + 5. Apoptosis -ve 6. DNA repair -ve | Potentially malignant lesions (Red and white lesions) | Oral carcinoma |
1. Destruction of cell-cell contact within the tumor
2. Attachment to matrix components
3. Degradation of extracellular matrix
4. Migration of tumor cells
1. Eliminate immunogenic subclones + selective outgrowth of antigen negative variants
2. Low expression of histocompatibility antigens (HLA class 1) – to escape T cell cytotoxicity – more susceptible to NK cells
3. Lack co-stimulatory molecules eg. B7
4. Secrete immunosuppressive agents eg. TGF beta
5. Kill T cells: melanomas and hepatocellular carcinomas express Fas-ligand – selectively kill T cells by apoptosis – when they come into contact
Steps:
1. Acquiring genetic mutations and epigenetic changes – occur over a widespread multifocal field – leads to molecular lesions
2. Progress to cytologically recognizable premalignant foci of dysplasia
Histological changes in epithelial dysplasia:
Architectural changes:
3. Progress to carcinoma in-situ
4. Progress to carcinoma
Normal cells —Initiation→ Initiated cells —Promotion→ Preneoplastic cells —Progression→ Neoplastic cells
Procarcinogen —Metabolic activation→ Genotoxic carcinogen → DNA damage —Proliferation→ DNA mutations —Proliferation→ Activate oncogene, inactivate tumor suppressors —Proliferation→ Tumor
Clinical:
Mechanism:
Diagnosis:
Management:
Rapidly spreading cellulitis involving submandibular, sublingual and submental spaces bilaterally
DentMistry 