1. DENTINAL SCLEROSIS ( TRANPARENT DENTIN / SCLEROTIC DENTIN )
1.1. regressive alteration of tooth substance that is characterized by calcification of the dentinal tubules
1.2. Etiology
1.2.1. Injury of dentin by caries or abrasion
1.2.2. Normal ageing process
1.2.3. Deposition of Ca salts in tubules
1.3. C/F
1.3.1. Increased mineralization of tooth
1.3.1.1. decreased conductivity of the odontoblastic processes
1.3.2. Slows advancing carious process
2. DEAD TRACTS
2.1. Seen in ground sections of teeth
2.2. odontoblast process disintegrate & empty space is filled with air
2.3. Manifested as a black zone by transmitted light but as white zone by reflected light
2.4. Due to difference in the refractive indices of the affected tubules & normal tubules
2.5. Tubules are not calcified
2.6. Permeable to penetration of dyes
3. SECONDARY DENTIN Physiological secondary dentin.
3.1. deposited after root formation is completed.
3.2. Represents continuing but much slower dentin deposition by odontoblasts after completion of root formation.
3.3. uniform layer of dentin around the pulp chamber.
3.4. Laid down throughout the tooth life
3.5. Produced more slowly than primary dentin
4. TERTIARY DENTIN
4.1. Produced in response to stimuli like attrition, caries or a restorative dental procedure.
4.2. C/F
4.2.1. Decrease in tooth sensitivity
4.2.2. Forms an insulating layer of calcified tissue between pulp & pathologic process
4.2.3. Anterior teeth exhibit higher incidence
4.3. R/F
4.3.1. Particularly in the pulp horn & teeth with proximal caries.
4.3.2. Decrease in size of pulp chamber & root canals.
4.4. H/F
4.4.1. decalcified stained sections, often exhibits a different tinctorial reaction.
4.4.2. Demarcated from primary dentin by a deeply staining ‘resting line’.
5. RETICULAR ATROPHY OF PULP
5.1. Degenerative or regressive changes of pulp, particularly when they occur as an age change in elderly persons.
5.2. Etiology
5.2.1. Improper fixation of tooth & pulp after extraction.
5.2.2. Autolysis of pulp tissue
5.3. H/F
5.3.1. Large vacuolated spaces in the pulp.
5.3.2. Reduction in no. of cellular elements.
5.3.3. Degeneration & disappearance of odontoblasts.
6. RESORPTION OF TEETH
6.1. Normal process in shedding of deciduous teeth.
6.2. begin either on the external surface (due to tissue reaction in periodontal or pericoronal tissue)
6.2.1. or inside the tooth (from pulpal tissue reaction).
6.3. Classifications
6.3.1. External
6.3.1.1. Periapical inflammation
6.3.1.1.1. Periapical granuloma due to pulpal infection or trauma causes resorption of root apex.
6.3.1.1.2. Occurs more readily in highly vascular areas
6.3.1.1.3. Appears as slight blunting of root apex.
6.3.1.1.4. Leads to severe loss of tooth surface.
6.3.1.1.5. Root canal fillings projects out from shortened roots.
6.3.1.2. Reimplantation of teeth
6.3.1.2.1. Results in severe resorption of tooth.
6.3.1.2.2. Analogous to bone graft, ultimately resorbed & replaced.
6.3.1.2.3. Produce ankylosis.
6.3.1.3. Tumors & cysts
6.3.1.3.1. appears due to pressure phenomenon.
6.3.1.3.2. Both benign & malignant tumor causes root resorption.
6.3.1.3.3. Connective tissue present between tumor & tooth develop osteoclast that do bone resorption.
6.3.1.4. Impaction of teeth
6.3.1.4.1. Destruction of epithelium, allows connective tissue to come in contact with crown, thus initiating resorption.
6.3.1.4.2. Also causes resorption of roots of adjacent teeth.
6.3.1.5. Excessive mechanical
6.3.1.5.1. Patient undergoes orthodontic treatment exhibit multiple areas of root resorption.
6.3.1.5.2. Resorption is mild & involves only a few teeth.
6.3.1.5.3. Appearance of small lacunae on the surface of cementum, extend into dentin, indicating early tooth resorption.
6.3.1.6. Idiopathic
6.3.1.6.1. Resorption of root in permanent teeth in normal adults is without any cause
6.3.1.6.2. exhibit resorption in four or more teeth
6.3.1.6.3. 82%- Men / 91%- Women
6.3.1.6.4. Related to one or more systemic disorder.
6.3.1.6.5. Begins near to cemento-enamel junction or near root apex.
6.3.1.6.6. Medically no past history.
6.3.2. Internal
6.3.2.1. Called:
6.3.2.1.1. Chronic perforating internal hyperplasia of pulp/Internal granuloma/Odontoclastoma/Pink tooth maummary
6.3.2.2. Etiology
6.3.2.2.1. Inflammatory hyperplasia of pulp.
6.3.2.2.2. Carious exposure.
6.3.2.2.3. Pulp infection
6.3.2.3. C/F
6.3.2.3.1. No clinical symptoms.
6.3.2.3.2. Appearance of pink hued area on crown of tooth.
6.3.2.3.3. Unusual for more than one tooth
6.3.2.3.4. No predilection for occurrence i
6.3.2.4. R/F
6.3.2.4.1. Tooth exhibits round or ovoid radiolucent area in central portion of tooth
6.3.2.4.2. Complete perforation if tooth left untreated.
6.3.2.5. H/f
6.3.2.5.1. Resorption of inner or pulpal surface of dentin.
6.3.2.5.2. Proliferation of pulp tissue.
6.3.2.5.3. Odontoclastoma’- Irregular lacunae show odontoclasts.
6.3.2.5.4. Pulp tissue exhibit chronic inflammatory reaction.
6.3.2.5.5. Lacunae are partially/completely filled with dentin.
7. CEMENTICLES
7.1. small foci of calcified tissue, lies free in periodontal ligament of lateral & apical root areas.
7.2. Calcified bodies occur in periodontal ligament.
7.3. Developed by calcification of nests of epithelial cells.
7.4. Imparts a roughened, globular outline to root surface.
7.5. Arise from focal calcification of connective tissue between Sharpey’s bundles.
7.6. Size 0.2-0.3mm in diameter.
8. Introduction
8.1. Regressive changes in the dental tissues include a variety of alterations.
8.2. Necessarily not related etiologically or pathologically.
9. ATTRITION
9.1. The physiological wearing away of a tooth as a result of tooth-to-tooth contact as in mastication
9.2. **This process is physiologic rather than pathologic
9.3. If the causes are:biting+bruxism ->
9.3.1. Now called Abrasion ***
9.4. Etiology
9.4.1. Physiological process
9.4.2. Age
9.4.3. Severe attrition – nail biting & bruxism
9.4.3.1. Remember (called Abrasion)
9.5. C/F
9.5.1. Occurs only on occlusal, incisal & proximal surfaces of teeth.
9.5.2. more in older persons.
9.5.3. More in men than women
9.5.4. Seen in both permanent & deciduous dentition.
9.5.5. Appears as small polished facet on cusp tip or ridge or slight flattening on incisal edge.
10. ABRASION
10.1. Pathological wearing away of tooth substance through some abnormal mechanical process.
10.2. Etiology
10.2.1. Use of abrasive dentifrice
10.2.2. Injudicious use of tooth brush
10.2.3. Habitual pipe smokers
10.2.4. Improper use of dental floss
10.3. C/F
10.3.1. V-shaped or wedge-shaped ditch on cemento- enamel junction of the tooth.
10.3.2. Gingival recession
10.3.3. Tooth root exposure
11. EROSION
11.1. Irreversible loss of dental hard tissue by a chemical process that does not involve bacteria.
11.2. Dissolution of mineralized tooth structure occurs upon contact with acids, introduced in oral cavity from intrinsic or extrinsic sources.
11.3. Etiology
11.3.1. Extrinsic causes
11.3.1.1. Acidic media either by way of food stuff or by iatrogenic exposure.
11.3.1.2. Very low pH fruits & fruit juices
11.3.1.3. Carbonated soft drinks
11.3.1.4. Medications that are acidic in nature
11.3.2. Intrinsic sources
11.3.2.1. Gastric acids regurgitation into oesophagus & mouth
11.3.2.2. Association with gastroesophageal reflux disease(GERD).
11.3.2.3. Chronic excessive vomiting
11.3.2.4. Anti-depressants causing salivary hypofunction
11.4. C/F
11.4.1. Wearing away of non occluding surface
11.4.2. Incisal grooving
11.4.3. Cupping of occlusal surface
12. PULP CALCIFICATION
12.1. Located in any portion of pulp tissue
12.2. More common in the pulp chamber & root canal
12.3. 66%- between age of 10-20 yrs
12.4. 90%- between age of 50-70 yrs
12.5. Classifications
12.5.1. Discrete pulp stone
12.5.1.1. True denticles
12.5.1.1.1. Types
12.5.1.1.2. localized masses of calcified tissue that resembles dentin because of their tubular structure.
12.5.1.1.3. More common in pulp chambers than root canal.
12.5.1.1.4. H/P
12.5.1.2. False denticles
12.5.1.2.1. Type
12.5.1.2.2. Composed of localized masses of calcified material.
12.5.1.2.3. Do not exhibit dentinal tubules.
12.5.1.2.4. Larger than true denticles.
12.5.1.2.5. Appears to be made up of lamellae or concentric layer of mineralization.
12.5.1.2.6. common in pulp chamber than in root canal.
12.5.1.2.7. When surrounded by secondary dentin, called as ‘Interstitial denticle’****
12.5.1.2.8. H/P
12.5.2. Diffuse calcification
12.5.2.1. Most commonly seen in root canals.
12.5.2.2. Calcification follows degeneration called as ‘calcific degeneration’.
12.5.2.3. Pattern is amorphous, unorganized linear
12.5.2.4. C/F
12.5.2.4.1. 66%- between age of 10-20 yrs.
12.5.2.4.2. 90%- between age of 50-70 yrs.
12.5.2.4.3. No difference in frequency between genders & various teeth
12.5.2.4.4. Dental pain
12.5.2.4.5. Difficulty in root canal therapy.
12.5.2.5. H/F
13. HYPERCEMENTOSIS (CEMENTUM HYPERPLASIA)
13.1. Non-neoplastic condition in which excessive cementum is deposited in continuation with the normal radicular cementum.
13.2. Etiology
13.2.1. Accelerated elongation of tooth.
13.2.2. Inflammation about tooth because of pulpal infection.
13.2.3. Tooth repair
13.2.4. Osteitis deformans or Paget’s disease of bone.
13.3. C/F
13.3.1. After extraction root appear larger in diameter than normal.
13.4. R/F
13.4.1. Thickening & apparent blunting of roots.
13.4.2. Exhibits rounding of the apex.
13.5. H/f
13.5.1. Excessive secondary or cellular cementum deposited directly over thin layer of primary acellular cementum
13.5.1.1. osteocementum
13.5.2. Cementum arranged in concentric layers around the root.
13.5.3. Shows numerous resting lines.