Non-apnea Sleep Disorder Increases the Risk of Periodontal Disease: A Retrospective Population-Based Cohort Study (Version 3).
ABSTRACT Aim: The aim of this study was to determine whether non-apnea sleep disorder patients with comorbidity have an increased risk of periodontal disease. Materials and Methods: Patients newly diagnosed with non-apnea sleep disorders (NA-SD) in 1997-2010 were identified as the study cohort from the Taiwan National Health Insurance (TNHI) database. For each NA-SD patient, two matched controls without sleep disorders were randomly selected for comparison. Results: The overall incidence rate ratio of severe periodontal diseases was 39% higher in the NA-SD cohort than in the without NA-SD cohort (7.93 vs. 5.69 per 1,000 person-years), with an adjusted HR of 1.36, (95% CIs = 1.30-1.43). The effect of NA-SD on the risk of severe periodontal diseases was higher in young patients, and middle-aged patients, as compared with patients over 65 years of age (≤ 35 years of age, HR = 1.13, 95% CIs = 1.04-1.24; 35-50 years of age, HR = 1.73, 95% CIs = 1.61-1.86; 50- 65 years of age, HR =1.69, 95% CI = 1.58-1.81). Conclusion: Non-apnea sleep disorder might increase the risk of periodontal disease.
- SourceAvailable from: James M Reuben[Show abstract] [Hide abstract]
ABSTRACT: The extent to which sleep loss may predispose astronauts to a state of altered immunity during extended space travel prompts evaluation with ground-based models. We sought to measure plasma levels of selected cytokines and their receptors, including the putative sleep-regulation proteins soluble TNF-alpha receptor (sTNF-alpha R) I and IL-6, in human subjects undergoing 2 types of sleep deprivation during environmental confinement with performance demands. Healthy adult men (n = 42) were randomized to schedules that varied in severity of sleep loss: 4 days (88 hours) of partial sleep deprivation (PSD) involving two 2-hour naps per day or 4 days of total sleep deprivation (TSD). Plasma samples were obtained every 6 hours across 5 days and analyzed by using enzyme-linked immunoassays for sTNF-alpha RI, sTNF-alpha RII, IL-6, soluble IL-2 receptor, IL-10, and TNF-alpha. Interactions between the effects of time and sleep deprivation level were detected for sTNF-alpha RI and IL-6 but not for sTNF-alpha RII, soluble IL-2 receptor, IL-10, and TNF-alpha. Relative to the PSD condition, subjects in the TSD condition had elevated plasma levels of sTNF-alpha RI on day 2 (P =.04), day 3 (P =.01), and across days 2 to 4 of sleep loss (P =.01) and elevated levels of IL-6 on day 4 (P =.04). Total sleep loss produced significant increases in plasma levels of sTNF-alpha RI and IL-6, messengers that connect the nervous, endocrine, and immune systems. These changes appeared to reflect elevations of the homeostatic drive for sleep because they occurred in TSD but not PSD, suggesting that naps may serve as the basis for a countermeasures approach to prolonged spaceflight.Journal of Allergy and Clinical Immunology 02/2001; 107(1):165-70. · 12.05 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Periodontitis is a chronic bacterial infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontitis principally through their effects on the normal immune and inflammatory mechanisms. Several conditions may give rise to an increased prevalence, incidence or severity of gingivitis and periodontitis. The effects of a significant number of systemic diseases upon periodontitis are unclear and often it is difficult to causally link such diseases to periodontitis. In many cases the literature is insufficient to make definite statements on links between certain systemic factors and periodontitis and for several conditions only case reports exist whereas in other areas an extensive literature is present. A reduction in number or function of polymorphonuclear leukocytes (PMNs) can result in an increased rate and severity of periodontal destruction. Medications such as phenytoin, nifedipine, and cyclosporin predispose to gingival overgrowth in response to plaque and changes in hormone levels may increase severity of plaque-induced gingival inflammation. Immuno-suppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune mechanisms (such as HIV infection) may predispose the individual to periodontal destruction. There is convincing evidence that smoking has a detrimental effect on periodontal health. The histiocytoses diseases may present as necrotizing ulcerative periodontitis and numerous genetic polymorphisms relevant to inflammatory and immune processes are being evaluated as modifying factors in periodontal disease. Periodontitis severity and prevalence are increased in diabetics and worse in poorly controlled diabetics. Periodontitis may exacerbate diabetes by decreasing glycaemic control. This indicates a degree of synergism between the two diseases. The relative risk of cardiovascular disease is doubled in subjects with periodontal disease. Periodontal and cardiovascular disease share many common risk and socio-economic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying aetiology of both diseases is complex as are the potential mechanisms whereby the diseases may be causally linked. It is thought that the chronic inflammatory and microbial burden in periodontal disease may predispose to cardiovascular disease in ways proposed for other infections such as with Chlamydia pneumoniae. To move from the current association status of both diseases to causality requires much additional evidence. Determining the role a systemic disease plays in the pathogenesis of periodontal disease is very difficult as several obstacles affect the design of the necessary studies. Control groups need to be carefully matched in respect of age, gender, oral hygiene and socio-economic status. Many studies, particularly before the aetiological importance of dental plaque was recognised, failed to include such controls. Longitudinal studies spanning several years are preferable in individuals both with and without systemic disease, due to the time period in which periodontitis will develop.Australian Dental Journal 04/2001; 46(1):2-12. · 1.37 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Evidence for the reciprocal role of the immune system in sleep is growing. Sleep disturbances are believed to be both a cause and a consequence of various immune and autoimmune conditions.Holistic nursing practice 01/2003; 17(2):65-80. · 0.34 Impact Factor