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Aging is associated with chronic low-grade increases in circulating levels of inflammatory markers. A wide range of environmental factors, including smoking, infections, and obesity, genetic factors, and the declining function of sex hormones may contribute to systemic low-grade inflammatory activity in older individuals. Age-associated disease may exacerbate this phenomenon. The multifunctional cytokines TNF-alpha and IL-6 have been associated with morbidity and mortality in the elderly. Evidence supports the direct role of TNF-alpha in the pathogeneses of atherosclerosis, type 2 DM, and AD in older individuals. Age-related increases in systemic levels of TNF-alpha could provide a unifying basis for these disorders. Furthermore, TNF-alpha induces a catabolic state that causes frailty. Circulating levels of IL-6 seem to be a strong risk factor for frailty in the elderly, which could reflect its association with increased production of TNF-alpha. IL-6 also may be a risk factor for thromboembolic complications. In healthy, elderly populations, high circulating levels of TNF-alpha and IL-6 predict mortality, independent of comorbidity, indicating that TNF-alpha and IL-6 cause morbidity and mortality. In cohorts of frail, older individuals, TNF-alpha and IL-6 also act as disease markers. Circulating levels of TNF-alpha seem to be the best predictor of mortality in frail, elderly populations with a high mortality rate, whereas IL-6 seems to be the strongest risk marker in healthy, elderly populations. This finding could reflect that in relatively healthy old populations the increase in circulating levels of IL-6 represent a systemic response to local proinflammatory activities; however, when age-related inflammatory diseases progress, levels of TNF-alpha increase in the circulation and become gradually a stronger risk marker than IL-6. In conclusion low-grade elevations in levels of circulating cytokines are strong independent risk factors of morbidity and mortality in the elderly, and lifestyle factors and comorbidities may modulate these levels. Exercise and dietary interventions may be possible strategies to decrease inflammatory activity and improve the health status of the elderly.
1. Six hundred patients in a private periodontal practice were reexamined an average of 22 years after their active treatment and the patterns of tooth loss were observed. 2. During the post-treatment period, 300 patients had lost no teeth from periodontal disease, 199 had lost one to three teeth, 76 had lost 4 to 9 teeth and 25 had lost 10 to 23 teeth. 3. Of 2,139 teeth that originally had been considered of questionable prognosis, 666 were lost. Of these, 394 were lost by one sixth of the patients and only 272 by the other five-sixths. 4. Of 1,464 teeth which originally had furcation involvements, 460 were lost, 240 of them by one-sixth of the patients who deteriorated most. 5. The mortality of teeth which were treated with periodontal surgery was compared with that of teeth which did not have surgery. Tooth retention seemed more closely related to the case type than the surgery performed. 6. In general, periodontal disease is bilaterally symmetrical and there is a predictable order of likelihood of tooth loss according to position in the arch.
The aim of the present investigation was to evaluate the periodontal conditions of a group of patients who, following active treatment of extremely advanced periodontal disease, had been maintained for 14 years in a well-supervised maintenance care program. The present sample included 61 subjects out of an initial group of 75 individuals who in 1969 were referred to and treated by the authors. Following an initial examination, the patients were given detailed instructions in proper plaque control measures and were subjected to scaling and root planning and surgical elimination of pathologically deepened pockets. After the termination of the active treatment phase, the patients were placed in a maintenance care program including recall appointments every 3-6 months. At the initial examination, immediately after the completion of the active treatment phase and then once a year, all patients were examined regarding oral hygiene, gingival conditions, probing depths and clinical attachment levels. In addition, the interproximal alveolar bone height was determined from full mouth radiographs obtained before active treatment, at the completion of active therapy and 1, 3, 5, 8, 10, 12 and 14 years after treatment. The results from the repeated examinations demonstrated that treatment of advanced forms of periodontal disease resulted in clinically healthy periodontal conditions and that this state of "periodontal health" could be maintained in most patients and sites over a period of 14 years. It was also demonstrated that the treatment and maintenance programs described were equally effective in young and older patients. The individual mean values describing probing depths, attachment levels, and bone heights did not vary significantly over the 14 years of observation. A more detailed analysis of the data revealed, however, that a small number of sites in a few patients lost a substantial amount of attachment. This attachment loss occurred at different time intervals during the course of the maintenance period. Thus, 43 surfaces in 15 different patients were exposed to recurrent periodontal disease of a significant magnitude. This recurrent inflammatory periodontal disease caused the loss of 16 teeth in 7 different patients during the maintenance period. The data reported question the validity of using individual mean values to describe alterations of the periodontal conditions during maintenance following active periodontal therapy.
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