DEPARTMENT OF PERIODONTICS

AGING AND PERIODONTIUM

PRESENTED BYBHRUGESH PANSERIYA

Aging and Periodontium

Introduction Effects of Aging on the Periodontium
Gingival epithelium Gingival connective tissue Periodontal ligament Cementum Alveolar bone Blood vessels

Effects of Aging on the Bacterial Plaque Effects of Aging on the Immune Response Effects of Aging on the Progression of Periodontal Diseases Effects of Aging on the Response to Treatment

Introduction
A variety of age related changes in the oral cavity and throughout the aging body can affect dental care and treatment plans. Today increased health awareness and preventive dentistry have led to decreasing tooth loss. So it is important to review aging effects and their clinical significance to the disease process and also their possible treatment outcomes. It is difficult to draw conclusions on the effects of aging.

Effects of Aging on the Periodontium

Gingival epithelium Thinning and decreased keratinization of epithelium reported with aging. Significance: - Increase in epithelial permeability to bacterial antigens. - Decreased resistance to trauma. Flattening of rete pegs and altered cell density. Some reports show migration of junctional epithelium to more apical position on the root surface. The width of attached gingiva should decrease due to recession but it usually increases with aging. The migration of junctional epithelium could be caused by passive eruption or may be due to cumulative effects of inflammation or trauma. Gingival connective tissue Daniel Grant and Sol Bernick stated that increasing age results in decrease in cellullarity, coarser and more dense gingival connective tissues. Clausen, Verzar, Gross and Milch stated that changes take place in the physical and chemical properties of collagen. - Increased conversion of soluble to insoluble collagen - Increased mechanical strength, a decrease in the extensibility and an increase thermal contraction of collagen. - Increased denaturing temperature. There is a decrease in the ratio of ground substance to collagen, a decrease in collagen turnover, and decrease in water content. Oliver

suggested that the loss of ground substance was due to a reduced supply of oxygen associated with altered arterial flow.

Periodontal ligament Decreased no. of fibroblasts and more irregular structure. Daniel Grant and Sol Bernick stated that principal fiber bundles were recognized thicker and cellularity was decreased. The areas between fiber bundles were reduced in size. Calcifications have been noted in the periodontal ligament as seen in pulp and other organs of the body. Other findings include decreased organic matrix production and epithelial cell rests and increased amounts of elastic fiber. The age changes in periodontium are similar to those described in other connective tissue of the body. Width of periodontal ligament will decrease if the tooth is unopposed or will increase with excessive loading. Cementum An increase in cemental width may be 5 to 10 times with aging because of continuous deposition of cementum after eruption. The increase in width is greater apically and lingually. Alveolar bone Morphologic changes in alveolar bone are similar to other bony sites in body. Sharpeys fibers were not demonstrated with silver nitrate impregnation stain. Daniel Grant and Sol Bernick stated that surfaces of alveolar socket showed little evidence of resorption and almost no apposition. It may be that physiologic tooth migration is slowed or even halted in old age, as remodeling of bone slows or ceases. Specific to periodontium are more irregular periodontal surface of bone and less regular insertion of collagen fibers. The healing rate of extraction sockets appears to be unaffected by increasing age.

Blood vessels In the gingival tissue the density of blood vessels was reported to be greater when 35 to 45 year old and 65 to 75 year subjects were compared to subjects aged 18 to 25 years, but the no. of vessels with active flow was decreased. Bacterial plaque Quantity Studies using the human experimental gingivitis model, introduced by Loe et al. (1965), have shown that, starting with a healthy gingiva, withdrawal of oral hygiene procedures led to increased amounts of bacterial plaque and the subsequent development of inflammation. Holm-Pederson et al suggested that accumulation has been suggested to increase with age due to - Increase in hard surface area as a result of gingival recession surface characteristic of exposed root surface as a substrate for plaque formation as compared to enamel. - Possible differences in dietary habits and age-related changes in salivary composition and flow rate may influence plaque formation. - Differences in bacterial composition of bacterial plaque may account for the increase in plaque quantity. In contrast study of Van der Velden et al. have shown no difference in plaque quantity with age. Regarding the development of plaque and swelling. A younger age group developed more inflammation in terms of bleeding on probing, than older age group. The rate of development of redness was significantly higher in the younger group. Quality Holm-Pederson et al suggested that the most conspicuous difference between the two age groups was the reduction in total no. of recoverable, viable microorganisms in plaque from elderly individuals coupled with a reduction in the levan hydrolase activity. It does not necessarily imply the presence of fewer bacteria. The reduced counts of viable microorganisms represent a shift from a predominantly facultative and aerobic flora to a predominantly anaerobic flora. Subgingival plaque Study of Van der Velden et al demonstrated no differences in plaque composition between two age groups whereas another study reported increased no. of enteric rods and pseudomonads in older adults.

These differences in the results of above stated study may be due to difference in case selection. Van der Velden et al selected cases with absence of gingival recession, since it is likely that plaque accumulates more rapidly on cementum than on enamel, because of difference in roughness of the tooth surface.

Immure responses - Recent advances in the study have altered the understanding of this phenomenon. As a result, age has been recognized as having much less effect in altering the host response than previously thought. - Differences between young and older individuals can be demonstrated for T and B cells, cytokines and natural killer cells but not for polymorphonuclear cells and macrophage activity. Age related decline occurs in the cellular arm of the immune response, whereas destructive periodontal disease is associated with the humoral arm of the immune response, which is less affected by age. McArthur concludes Measurement of indicators of immune and inflammatory competency suggested that, within the parameters tested, there was no evidence for age related changes in host defenses correlating with periodontitis in an elderly (65 to 75 years) group of individuals, with and without disease Holm-Pederson and associates reported that older subjects demonstrate diminished cellular immune response develop gingival inflammation more rapidly than younger subjects. Older subjects developed gingival inflammation more rapidly than and with greater severity than younger subjects in an experimental gingivitis model. Age related differences in the inflammatory response in gingivitis have been clearly demonstrated. In summary some age related changes are evident in the periodontium and host response. Effects of aging on the progression of periodontal diseases In the experimental gingivitis study comparing younger and older subjects greater inflammatory response is observed in older subjects. They demonstrated greater size of infiltrated connective tissue, increased gingival crevicular fluid flow and increased gingival index. Loss of attachment Age is associated with an increased loss of connective tissue attachment might reflect cumulative exposure to no. of potentially destructive processes.

These might include - Plaque associated periodontitis, - Chronic mechanical trauma from tooth brushing and Iatrogenic damage from unfavorable restorations or repeated scaling and root planing. The conclusion of different studies show that the effect of age is either nonexistent or provides a small and clinically insignificant increased risk of loss of attachment. So age has been suggested not to be a true risk factor but a background or an associated factor for periodontitis. Effects of aging on the response to treatment of the Periodontium The successful treatment of periodontitis requires both meticulous home care control by the patient and meticulous supragingival and subgingival scaling by therapist. Studies have demonstrated that despite the histologic changes in the periodontium with aging, no differences in response to non surgical or surgical treatment have been shown for periodontitis. Although aging does not appear to affect outcome of periodontal therapy, age is very important factor that should always be considered when assessing patient susceptibility. The prognosis of 25-year aged patient with generalized moderate chronic periodontitis is less favorable than the prognosis of a 55-yr old patient with similar environment risk factors and extent of periodontal destruction.

Effect of age on healing following periodontal therapy It has been well documented that the rate of healing of skin wounds is deceased and the tensile strength development of skin incision wounds retarded due to aging. Finding describing the influence of age on wound healing in the periodontium are somewhat conflicting.

Holm-Pederson & Loe (1971) studied wound healing in the gingiva of young and old human volunteers. - A 2-mm biopsy was performed in a standardized way and healing monitored for a period of 2 to 10 months. They reported that healing occurred faster in the young individuals. - The most conspicuous difference was that the free gingiva of young adults regenerated to pre operative levels within 60 days, that of old individuals never did regenerate completely.

Abbas et al. (1984) reported that younger and older patients with same degree of periodontal tissue breakdown were treated for their periodontal conditions with surgical pocket elimination and placed on plaque control program. At the re examination 5-15 weeks after surgery, the younger patients showed more bleeding pockets than the older patients. They concluded that as younger patients are more susceptible to periodontal disease than older patients with same attachment loss, the time span for wound healing is longer in patients who are more susceptible (young patients) to periodontal disease, than in those who are less susceptible.

Study by Lindhe and Nyman(1984) failed to demonstrate that the age of patients with moderately advanced or advanced forms of periodontal tissue breakdown had an influence on healing of the periodontal tissues following treatment or on the incidence of recurrent disease. - 2 samples of patients with different degrees of periodontal disease were included in the study. Sample A- Moderately advanced periodontal disease, with age difference between younger and older patients was 20 years or more. Sample B- Patients with advanced destruction of the supporting apparatus, age difference between younger and older patients were at least 30 years. Both in sample A and B, the periodontal tissue alteration studied (gingivitis, probing pocket depth and probing attachment level) before and after treatment appeared to be similar in young and old patients. Both younger and older groups responded to active therapy with the same degree of gingivitis resolution, probing depth reduction and attachment level change.

These findings may appear to variance with results reported by Abbas et al. (1984) who observed that during a period of 5-15 weeks after periodontal surgery, younger patients had more bleeding pockets than older patients. It should be realized that the first re-examination of sample A in the present material carried out 6 months after the end of active therapy. In sample B during the 14 years of maintenance therapy, the younger and older patients demonstrated a similar low tendency to develop recurrent disease. Another finding in this study was that buccal sites of older subjects showed less probing depth reduction and lost more probing attachment

than younger individuals are in accord with the investigation of HolmPederson & Loe (1971) of wound healing in the gingiva of young and old individuals. They demonstrated that regeneration of the buccal tissues after a standardized biopsy procedure was more rapid and complete in young than old subjects.

A purely physiologic and biologic review indicates that the effects of aging on the structure of the periodontium, function of the immune response and nature of either supragingival or subgingival plaque have a negligible impact on an individuals experience of periodontal diseases.