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Age changes in enamel, dentin and pulp1.pptx
- 1. Age Changes inEnamel, Dentin and Pulp
- 2. • Ageing isdefined as a process of morphological and physiological disintegration as distinguished from infant, childhood and adolescence which are typified by processes of integration and coordination. Carranza.
- 3. Major Tissues ofthe Tooth The completely formed teeth and the periodontium should remain intact and fully functional without disease for a lifetime.
- 4. Age changes inEnamel MACROSCOPIC -Becomes darker -Attrition, Abrasion, Erosion -Longitudinal cracks MICROSCOPIC - Decreased - enamel rod ends - perikymata - permeability to fluids - Increase in nitrogen and fluorine • Increased resistance to decay
- 5.
- 6. COLOUR • Becomes darkerwith age. • Associated with changes in the organic portion of enamel, presumably near the surface.
- 7. ATTRITION ,ABRASION ANDEROSION Attrition Abrasion Erosion
- 8. ATTRITION • Physiologic wearof the occlusal surfaces and proximal contact points as a result of mastication. • Evidenced by a loss of vertical dimension of the crown and by flattening of the proximal contour. Causes • Masticatory stress • Para-functional habits
- 9. Stages of Attrition StageI- Wear of enamel at cusps and incisal edges without exposure of dentin. Stage II Wear of enamel and exposure of dentin on incisal edges and isolated area over individual cusps. Stage III Wear of enamel forming a broad strip on incisal edges and the confluence of two are more areas of wear over adjacent cusps. Stage IV Wear of enamel and dentin on incisors to form a plateau on the teeth to form a central area
- 10. ABRASION • Pathological wearingaway of tooth through abnormal mechanical processes. e.g.- abrasive dentifrice - occupational - improper flossing
- 11. EROSION • Loss oftooth substance by a chemical process that does not involve known bacterial action. • Lingual erosion e.g. -chronic vomiting -acidic carbonated beverages
- 12. LONGITUDINAL CRACKS • Maybe developmental in origin. • Although their numbers do not increase with age , they become more obvious.
- 13. Site-specific thickness of enamel •Thinningof enamel at the level of cementoenamel junction. • Thickening at the incisal edge (maximum facial-palatal width) due to wear with advancing age. •These phenomena results in an overall decrease in the
- 14.
- 15. PERIKYMATA • Transverse wavelike grooves which lie parallel to each other and also to cemento -enamel junction. • The surfaces of unerupted and recently erupted teeth are covered completely with pronounced rod ends and perikymata. • Advancing age shows generalized loss of rod ends and slower flattening of perikymata which are eventually lost. • More rapid loss of structure Facial and lingual surfaces Anterior teeth
- 17. PERMEABILITY TO FLUIDSAND WATER CONTENT Due to acquisition of ions from oral fluids. Crystal size increases Reduction in pore size within the substance of enamel. Decrease in permeability and water content
- 18. Continuous deposition of fluorideand nitrogen on enamel surface Increase in fluoride concentration of enamel Increased resistance to decay Hardness and Elastic modulus of enamel increases . Increases the brittleness of teeth and decreases permeability. Cracks
- 19. Age changes inDentin • Two major changes in dentin: • Formation of secondary dentin. • Sclerosing or obturation of the dentinal tubules. A- dead tract B- sclerotic dentin
- 20. Secondary dentin • Secondarydentin forms after the complete formation of the tooth. Types: • Physiologic secondary dentin, which forms with normal stimulus, • Reparative secondary dentin, which forms with traumatic or abnormal stimulus.
- 21. Types of secondarydentin Regular Cause: mild stimuli (slow attrition, slowly progressing caries) Site of formation: entire pulpal surface (thicker on pulp roof and floor) Tubules: wavy course, decrease in number Clinically: The increase of the dentin thickness and the closure of the pulp horns make it much less possible to expose the pulp chamber during preparation. Irregular Cause: severe stimuli, severe attrition, erosion, deep caries. Site of formation: localized (eg pulp horn) Tubules: wavy and twisted course, decrease in number or atubular Clinically: Functions as a barrier for against caries.
- 22. Physiologic regular secondarydentin Secondary D Primary D
- 23. Odontoblas ts are cut Degenerate Replacedby the migration of undifferentiated cells from cell rich zone Odontoblasts are cut Live odontoblast s Reparative Dentin Reactionar y/Regenera ted Dentin Extensiv e abrasion , Erosion ,caries REPARATIVE /REACTIONARY DENTIN
- 24. DEAD TRACTS • Odontoblasticcell processes in the dentinal tubules are degenerated, leaving behind empty, air-filled tubules referred to as “dead tracts”. • Appear black in transmitted light and white in reflected light. • Probably the initial step to form sclerotic dentin. • Demonstrate decreased
- 25. TRANSLUCENT OR SCLEROTICDENTIN • Physiological change or pathological change (caries, attrition, deep fillings, ) in primary or secondary dentin. • More highly mineralized, harder and denser than normal dentin • Seen first near the root apex in a middle aged person. • Spreads upwards from the apex with advancing age. • This is one of the criteria used in forensic Young dentin Adult dentin Sclerotic denti
- 26. Sclerotic dentin Appears lightin transmitted light and dark in reflected light
- 28. Decrease in sensationto hot and cold stimuli. Tubular lumen becomes obturated by peritubular dentin. By age 80, almost all dentinal tubules are fully occluded. Secondary dentin grows inwardly into the pulp chamber decreasing the chamber’s size . Age related Sensitivity changes
- 29. Age changes inthe pulp • Reduction in the size and volume of the pulp as a result of a continuous deposition of dentin. • Decrease in the number of cells and apparent increased fibrosis with time, may not be from continued formation of collagen but may be due to the persistence of connective tissue sheath in an increasingly narrow pulp space.
- 30. • Cellular compositionof the pulp is modified. • Fibroblasts and Odontoblasts show degeneration with decrease in size and decrease in the number of cell organelles. • Ultrastructural studies reveal an increase in vacuole numbers and gradual degenerative changes leading to the
- 31. Changes in vasculardistribution: • There is a narrowing of the circumference of the blood vessels. • Atherosclerotic changes are seen in small arteries in the root pulp of aging teeth. • Intimal layer of the vessel is thickened resulting in a small lumen.
- 32. Changes in nervedistribution: • Degeneration and loss of pulpal nerve fibres may affect transmission from pulpal structures, resulting in increased thresholds to pain stimuli. • Myelin sheath changes and terminal axon remolding due to age related axon injury could be sources of abnormal pain in the oral region.
- 33. Pulp stones • Theseare nodular, calcified masses appearing in either or both the coronal or root portions of the pulp organ. • True -Made of dentin and lined by odontoblasts ,found close to root apex • False -Formed from degenerating cells which mineralize, usually found in the pulp chamber
- 34. Free -Stone notrelated to pulp space wall, surrounded by soft tissue. Adherent -Stone attached to wall of pulp space, not fully enclosed by dentin. Embedded -Stone enclosed within canal wall.
- 36. • Fibrodentine -Materialproduced by fibroblast-like cells against dentin prior to differentiation of a new generation of odontoblast-like cells. • Dystrophic calcification -Inappropriate biomineralization of the pulp in the absence of mineral imbalance.
- 37. Root Caries: AnEpidemic of Aging Teeth • Root caries, a pathologic process, occur with greater frequency in older adults than in any other age groups. • Xerostomia, a common symptom in older adults, along with cementum loss, gingival recession, poor oral hygiene, high plaque, and periodontal disease increase risk for root caries. • Asyptomatic but if left untreated, root caries can progress into pulpal infection resulting in local infection of
- 38. ENDODONTIC CONSIDERATIONS • Formationof a permanent tooth generally completes in three years after its eruption into the oral cavity but this doesnot apply to maturation of apex. • Remodeling/deposition of the cementum occuring at the apex is an aging process. • This probably occurs to compensate for the attrited enamel, or due to physiological mesial
- 39. • As asequelae to depostion, there is an increase in the overall distance from the root apex to the apical constriction of the root canal. • Working length of a tooth is relatively shorter from the radiographic apex for an aged tooth than it is for a young adult. • Diameter of the apical foramen does not change with age.
- 40. • D. Arola,R.K. Reprogel carried out a study to evaluate effects of aging on the mechanical behavior of human dentin and concluded : • The maximum flexure strength and energy to fracture dentin decreases with age. • The mean flexural strength of dentin beams from the youngest patients (17) exceeded 140MPa, whereas dentin beams from the oldest patients exhibited a mean strength of less than 80MPa. • There is a reduction in the fatigue strength of dentin and becomes more brittle with age.
- 41. • The olddentin was less tolerant to damage than young dentin. • Microcracks were more prevalent in young dentin and provided evidence of an increased ability to withstand fatigue damage. • Based on differences in the stiffness history and microcrack density, aging appears to result in an increase in both the rate of damage initiation and propagation in dentin.
- 42. Summary • Although thedentinal thickness may aid in pulpal protection, the pulp itself decreases in its reparative capabilities with age. • The pulpal blood flow declines due to a decrease in the number of blood vessels, and an increase in calcified tissues in pulp. • MRI findings suggest a decline in pulp signal intensity.
- 43. • Pulp stones,benign masses of mineralization within the pulp chamber, occur in approximately 6–7% of normal pulp in older adults. • The results of these physiologic changes along with dentinal thickness decrease pulpal resiliency and its ability to sense insult.
- 44. REFERENCES • Orbans textbookof oral histology and embryology 12 th edition. • Pathways of pulp by Stephen Cohen : 9th edition. • Normal Aging of Teeth Gregory An, Biology of Aging. • Effects of aging on the mechanical behavior of human dentin D. Arola, R.K. Reprogel. Biomaterials 26 (2005) 4051–4061
- 45. • Age-related transparentroot dentin: mineral concentration, crystallite size, and mechanical properties. J.H. Kinneya,, R.K. Nallab, J.A. Poplec, T.M. Breunigd, R.O. Ritchieb • Sex- and Age-related Differences in Primary and Secondary Dentin Formation. U. Zilberman, P. Smith • Pulp stones: a review R. Goga1, N. P. Chandler2 & A. O. Oginni3. International Endodontic Journal, 41, 457–468, 2008