Introduction to the effects of aging on the periodontium

Aging effects all the organ systems in the body and oral tissues are no exception to it. Due to widespread awareness regarding oral health, there has been an improvement in the oral health status of the general population worldwide. However, the process of aging is a natural process and sooner or later it affects various tissues in the body. The moderate loss of periodontal bone support can be related to the natural aging process; however, severe bone and attachment loss relate to periodontal disease-related tissue breakdown and should not be considered to be related to aging. It has been demonstrated that aging results in histopathological and clinical alterations in the oral tissues 1; however, these alterations should be distinguished from the pathological changes.

Effects of aging on periodontal tissues

As discussed in the normal periodontium, the periodontium consists of the gingiva, periodontal ligament (PDL), cementum and alveolar bone. All these tissues are subjected to changes associated with aging.

Age-related changes in gingiva:

The gingiva is exposed in the oral cavity and is primarily composed of epithelial tissue and connective tissue. With increasing age, there is thinning of epithelium and reduction in the keratinization of the gingival epithelium. There is also a reduction in the stippling of the attached gingiva with age. The rate of cell division in the basal layer of the gingival epithelium has not been shown to alter with increasing age; however, the cellular turnover rate does slow down for all regions of the oral cavity. Hence, there is a decline in the production of both young cells and fibers in the gingiva. The epithelial density has been shown to be increased with age 2; however, the morphology of cells does not change with age.

     There are changes in the structural organization of the epithelium and connective tissue. Changes in the shape of the retepegs have been reported with conflicting results. Both flattening of retepegs 3 and an increase in the height of the epithelial ridges 4 has been reported. A study analyzed the three-dimensional morphology of the epithelial-connective tissue interface, revealing that in young individuals, connective tissue ridges predominate whereas, in older individuals, connective tissue papillae predominate 5.

     The texture of the connective tissue changes with aging. In a study, it was shown that the connective tissue in younger individuals is finely textured and with aging, it becomes more coarse 4. The cellular composition of the connective tissue also changes with age. The primary cells in the gingival connective tissue are fibroblasts. It has been demonstrated in various in vivo and in-vitro studies that there is a structural as well as functional alteration in the fibroblasts with increasing age 6-9. In general, the number of cellular components of the connective tissue decreases with age. Furthermore, it has been demonstrated that with increasing age, the synthesis of collagen decreases 10. The differences have been found in protein synthesis by fibroblasts in …….. Contents available in the book……… Contents available in the book……. Contents available in the book……. Contents available in the book………..

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Age-related changes in the periodontal ligament (PDL)

The function of PDL is to act as a cushion between the occlusal forces and alveolar bone. PDL is primarily composed of fibroblasts, cementoblasts, osteoblasts, osteoclasts, Malassez epithelial rests and collagen matrix. The collagen matrix of PDL has collagen Type I and Type III as its major components. PDL is a dynamic tissue and its cells are involved in the repair of cementum, alveolar bone, and PDL itself. Aging affects the cellularity of PDL. A decreased cellularity has been demonstrated in PDL of older individuals as compared to younger individuals. Along with the decreased cellularity, the fiber content of PDL is also reduced. The structure of PDL becomes more irregular with increasing age 26-28. With advancing age, degenerating hyaline changes can be observed in PDL. Calcified bodies can also be observed in PDL and the epithelial rests show altered aggregation. The amount of organic matrix decreases with advancing age, whereas the amount of elastic fibers increases. The vascularity of PDL also reduces with age.

     Biochemical analysis demonstrates a decrease in the acid mucopolysaccharide content of the PDL with increasing age 27. A study, which analyzed collagen content derived from extracted human teeth demonstrated that there is a decrease in the amount of soluble collagen with increasing age 29. One explanation for this finding is, with increasing age, there is an increased cross-linking of the collagen fibers, resulting in reduced collagen solubility. However, there is an insufficient scientific support for this explanation. Another explanation for reduced collagen solubility is based on a change in the type of collagen synthesis by fibroblasts with increasing age. This explanation is supported by the findings made by Mayne et al. (1976) 30 on chondrocytes. They found that normally, chondrocytes synthesize collagen Type II, but as they grow older, they synthesize collagen Type I. One more explanation for the reduced collagen solubility is the increase in elastin fibers in the PDL in older individuals 31. With increasing age, there is a reduction in the mobility and chemotactic ability of PDL cells. In one study, reduced osteoclast chemotaxis and reduced rate of osteoclast differentiation were observed in samples derived from older individuals as compared to samples obtained from younger individuals 32. These findings may be associated with a reduced expression of the c-fos ligand by senescent cells 33.

     There are conflicting results regarding the changes in the width of PDL with aging. Some authors have reported an increase in the width of PDL with increasing age 34, 35 whereas; some others have reported a decreased width of PDL with increasing age 36, 37. However, the increase or decrease in the width of PDL can be explained on the basis of occlusal load on the teeth. It is well known that PDL space of non-functioning (hypo-functioning) teeth is narrower than the functioning teeth 38, 39. Due to tooth loss with the increasing age, the occlusal forces are increased on remaining teeth. This explanation could explain an increase in the width of PDL space of reaming teeth. On the other hand, a depressed occlusal function in older individuals may result in decreased PDL width. Thus, it can be summarized that if no teeth are lost, with increasing age, there is a decrease in the PDL space 40. Further, the width of the socket, as well as cementum, increases with age, which can also contribute to a narrower PDL space in older individuals 37.

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Physiological or pathological apical migration of junctional epithelium with advancing age:
It is well established that the presence of plaque is the primary etiology of periodontal breakdown which is determined by the apical migration of junctional epithelium (JE) from the cementoenamel junction (CEJ). Various studies have demonstrated an increased periodontal breakdown with age 13-16. Apical migration of JE due to inflammation, mechanical trauma (faulty tooth brushing) or anatomical position of the tooth in the arch have been well documented, but there is a controversial observation regarding physiological apical migration of JE in the healthy periodontium.

     According to some researchers, there is a physiological apical migration of JE due to continuous passive tooth eruption 17-19. This continuous passive tooth eruption occurs throughout the lifetime of an individual to compensate for the occlusal wear. Due to the continuous eruption, the CEJ of the tooth moves incisally/occlusally, but the location of the gingival margin remains constant, resulting in the apical migration of JE. In contrast to the continuous tooth eruption theory, results from other studies 20-22 suggest that there is no apical migration of the JE if the periodontium remains absolutely healthy. This hypothesis is based on two observations. One, the position of the mucogingival junction does not change with the advancing age 23 and two, the width of gingiva increases with advancing age in the absence of any pathological gingival recession 24, 25. As the gingival width increases with age, it seems likely that the position of JE remains at CEJ and there is no apical migration of JE with advancing age.

Age-related changes in cementum

Cementum is a thin layer of calcified connective tissue, covering the root surfaces of the teeth. Its formation on the root surface occurs throughout life 41, 42. Hence, the thickness of cementum increases throughout life. Although, cementum deposition takes place on all the surfaces of the root, but there is more cementum deposition in the apical region of the root 43. In one animal study, cementum deposition was found to be more on the lingual surfaces of the roots as compared to other surfaces 37. According to Severson et al. (1978) 44, greater cemental apposition in the apical region is a response to the passive eruption of the tooth. The process of passive eruption is coupled with the re-attachment of PDL fibers with cementum. Greater cementum deposition in the apical region of the tooth may be required to achieve this function. The course in which the fibers are embedded in cementum depends on the direction of forces the tooth is subjected to, during the formation of cementum 45.

     Cementum undergoes limited remodeling as compared to PDL and alveolar bone. The cementoblasts which deposit cementum, become entrapped within the cementum matrix and are then referred to as cementocytes. These cementocytes get deprived of the nutritional supply as the thickness of the cementum increases and ultimately they die. The cellular cementum is usually found at the root apices and in the furcation areas of multirooted teeth. With advancing age, cementum becomes acellular. Along with this, with advancing age, areas of cementum resorption followed by new cementum apposition can be observed, which may result in the irregular surface of cementum 40, 46.



Age-related changes in alveolar bone

In general, there is a decline in the rate of bone formation with advancing age, resulting in the reduction in bone mass 47. The bone metabolism is under the control of various mechanisms, including hormonal controls (parathyroid hormone, calcitonin, and estrogen) and non-hormonal controls (vitamin D metabolites, calcium, and phosphate concentration in plasma, growth factors and cytokines) 48.
     In animal studies, a decrease in the width of the cribriform plate has been observed with advancing age 27. Furthermore, the width of the interdental septum has also been demonstrated to decrease with advancing age in animals 49. However, these results have not been confirmed in humans. The interproximal wear of teeth may be related to the decreased width of the interdental septum. The cellular density of bone remodeling cells is also affected by advancing age. Severson et al. (1978) 44 demonstrated a decrease in the cells in the osteogenic layer of bone with advancing age.

Changes in endocrine profile with advancing age

The alteration in the endocrine profile of an individual with advancing age is an important factor associated with the aging process. Systemic deficiency of vitamin-D with advancing age is commonly found in community-dwelling elderly persons. Low serum calcium levels associated with vitamin D deficiency in association with renal insufficiency results in secondary hyperparathyroidism 50. These alterations lead to the mobilization of calcium ions from the bones, resulting in reduced osseous density. In post-menopausal women, due to reduced estrogen levels, osteoporosis is a common finding. Osteoporosis and Osteopenia have been considered as risk factors for periodontal bone loss 51, 52. Studies have demonstrated that female patients with Osteoporosis/ Osteopenia have a greater alveolar bone loss as compared to females with normal bone mineral density 53, 54.

Effects of advancing age on inflammatory response

In general, there is a gradual deterioration of the immune response associated with the natural process of aging. This process is referred to as “immunosenescence”. As we know, inflammation is a protective response which is generated when there is an injury to any tissue. The inflammatory response has been shown to be altered in advanced age. The term “inflammaging” …….. Contents available in the book……… Contents available in the book……. Contents available in the book……. Contents available in the book………..

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Altered cytokine profile with advancing age

It has been demonstrated that in elderly individuals, the systemic levels of inflammatory markers such as C-reactive protein, IL-6, and TNF are increased 58. However, it is debatable that whether chronic inflammatory diseases are the result of inflammaging or inflammaging is the result of chronic inflammatory diseases, or both are a cause and a consequence of each other in a vicious cycle.
     It should be emphasized here that even in the absence of any underlying disease, the levels of circulating cytokines (such as IL-1β, IL-6, and TNF) and acute-phase proteins (such as C-reactive protein and fibrinogen) have been found in elevated levels in elderly individuals 59, 60. Also, with advancing age, the levels of reactive oxygen species are elevated in the body. According to one hypothesis, oxygen-free radicals are the major contributors to the aging process 61. These may directly or indirectly contribute to a heightened inflammatory response in elderly individuals.
     Prostaglandin E2 (PGE2) is an arachidonic acid metabolism product. Increased levels of PGE2 have been shown to be positively associated with the alveolar bone loss in periodontitis cases 62, 63. In an animal study, it was demonstrated that IL-1β and PGE2 production from fibroblasts obtained from older mice (20 months of age) was significantly greater than fibroblasts obtained from younger mice (6 weeks) 64. Furthermore, increased synthesis of PGE2 and COX-2 mRNA has been demonstrated by PDL cells from elderly donors, when stimulated by bacterial LPS and mechanical stress, respectively 65, 66.

Changes in plaque composition with aging

As soon as the tooth surface is cleaned, it is covered by dental pellicle which acts as the foundation for plaque formation. If left undisturbed, the plaque formation and maturation occur on the tooth surface and within a few days, mature plaque develops on the tooth surface. A few studies have been done to compare the plaque composition in young and elderly persons. In one study, Holm-Pedersen et al. (1975) 67 compared the plaque in young and older individuals 20-24 years and 65-81 years of age, respectively, in an experimental gingivitis model. The results of the study demonstrated an increased plaque accumulation in the older age group than the younger age group. This difference was suggested to be due to the presence of recession and age-related changes in salivary flow in the older age group. In a subsequent study 68, authors analyzed the biochemical composition of plaque in the two age groups, determining the dextran hydroxylase, sucrase, levan hydro-lase and amylase activity. The levan hydroxylase activity was found to be markedly elevated in younger age group while other three enzymes demonstrated no significant activity difference between the two groups.

     The biochemical composition of the plaque was analyzed in one study where it was found that the calcium and phosphorous levels in adolescents were less as compared to adults 69. Cole et al. (1981) 70 analyzed …….. Contents available in the book……… Contents available in the book……. Contents available in the book……. Contents available in the book………..

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Effects of aging on wound healing

In general, the wound healing is delayed in elderly individuals as compared to young individuals. However, in healthy elderly people, there is no impairment of wound healing in terms of the quality of healing 72. The delayed wound healing in elderly individuals is due to an altered inflammatory response that includes delayed T-cell infiltration into the wound area with alterations in chemokine production and reduced macrophage phagocytic capacity 73. Other factors associated with delayed wound healing in elderly individuals include increased platelet aggregation, increased secretion of inflammatory mediators, decreased secretion of growth factors, impaired macrophage function, delayed re-epithelialization, delayed angiogenesis, delayed collagen deposition and reduced collagen turnover 72. Because of all these alterations, a reduced wound strength is observed in elderly individuals.

Aging as a risk factor for periodontitis

From the above discussion, it is clear that aging can be considered as a risk marker for periodontal disease progression. Various longitudinal studies have demonstrated a significant relationship between age and attachment loss or bone loss 74-76. However, the relationship between attachment loss and age is not linear. Although, some moderate amount of periodontal bone loss can be considered as a natural process, but aging does not result in advanced loss of periodontal support. As discussed in the previous section, alteration in the levels of various chemical mediators further contributes to periodontal disease progression. Elderly patients should be advised to maintain a good oral hygiene so that a healthy periodontium can be maintained.



Conclusion

Aging is a natural process and it affects the periodontium in the same way as it affects other parts of the body. However, aging itself does not lead to a severe loss of periodontal support. An altered immune response and altered healing have been observed in elderly individuals, which affect the periodontal disease progression. Good oral hygiene and strict adherence to the periodontal maintenance schedule significantly improves the long-term health and stability of the periodontium.

References

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