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PubMed1995

Diagnostic tests for periodontal disease activity.

Destructive periodontal disease is found in a significant number of adult patients. At present there is no reliable method of determining the presence of active periodontal disease, other than retrospectively. Tests are being developed that rely on various markers of periodontal disease activity but all of those produced to date have limitations. It is to be hoped that reliable tests that can be used at the chairside will help the general dental practitioner to combat periodontal disease before it progresses too far.

Adult↗
PubMed1983

Endocarditis prophylaxis for patients with periodontal disease.

Since periodontal disease provides a portal of entry for oral microorganisms during such common events as toothbrushing and mastication, treatment must resolve the inflammatory response if the teeth are to be maintained safely in patients at risk of infectious endocarditis. Prophylactic antibiotics should be administered during periodontal treatment such as debridement of the periodontal pocket and surgical repair of anatomic defects, as well as during oral hygiene training. If optimal periodontal health is achieved and maintained, the risk of systemic bacteremia is minimal.

Adult↗
PubMed1981

Fibrinolytic activity in periodontal disease. The relationship between fibrinolytic activity and severity of periodontal disease.

IN RECENT YEARS, evidence has evolved that suggests a relationship between fibrinolytic phenomenon and various inflammatory diseases. Plasmin activity and the response of the fibrinogen and fibrin degradation products latex test (FDPL test) in gingival fluid, along with plasminogen activator activity in gingival tissue were assessed. Samples were taken from periodontally involved persons and compared with healthy individuals. The following conclusions could be drawn: (1) The fluid from inflamed gingival crevices possessed more plasmin activity than that from clinically healthy crevices. The reaction of the FDPL test was stronger in the former. (2) Plasminogen activator activity in gingival tissue showed no significant difference between periodontally involved and healthy subjects.

Alveolar Process↗
PubMed1994

HIV disease as a risk factor for periodontal disease.

A multitude of oral lesions, including unique forms of periodontal disease, have been discovered in individuals infected with the human immunodeficiency virus (HIV). Although the frequency of HIV-associated periodontal diseases appears to be less than previously thought, many researchers agree that an important factor influencing the prevalence of unique periodontal disease in the HIV population is the degree of immunodeficiency. The pathogenesis of HIV-associated periodontal diseases remains unclear, but may be the result of microbiota and/or alterations in the host. HIV-gingivitis, now called linear gingival erythema, and HIV-periodontitis, now called necrotizing ulcerative periodontitis, have microbiology profiles similar to conventional adult periodontitis, although these lesions are quite different clinically. This article reviews clinical signs and symptoms, treatments, and the pathogenesis of HIV-related periodontal findings. It specifically focuses on the immuno-incompetence of HIV disease as a risk factor for periodontal disease. Because the caseload of acquired immunodeficiency syndrome patients will increase significantly in the future, the dental practitioner must be able to recognize and manage the periodontal lesions associated with HIV infection.

Dental Care for Chronically Ill↗
PubMed2005

Chronic glycine treatment inhibits ligature-induced periodontal disease in Wistar rats.

OBJECTIVE: Dysregulation of immune and stress responses plays a significant role for the development and progression of inflammatory diseases, including periodontal disease. The non-essential amino acid glycine modulates immune and central nervous system (CNS) responses, and has been shown to beneficially affect tissue destructive inflammatory conditions. The purpose of this study was to test the ability of orally administered glycine to influence periodontal disease progression, as well as immune and hypothalamic-pituitary-adrenal (HPA) responses following lipopolysaccharide stimulation. METHODS: Glycine was supplied in the drinking water during the whole experiment to male Wistar rats, starting 3 days before the induction of experimental ligature-induced periodontal disease. Control rats were given tap water only. The periodontal breakdown was assessed after the ligatures had been in place for 34 days. Following intraperitonal lipopolysaccharide stimulation, concentrations of the proximal cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin-10, as well as the HPA axis-derived hormone corticosterone, were measured in blood serum. RESULTS: Orally administered glycine significantly reduced periodontal bone loss as measured by digital X-rays (p = 0.007). Bone loss was negatively correlated with increased serum glycine, whereas no significant relationship was found with TNF-alpha, interleukin-10, or corticosterone. CONCLUSION: Chronic ingestion of glycine supplied in the drinking water significantly reduced periodontal bone loss. No effect of glycine on immune and HPA-axis responses was revealed. Further studies are needed to clarify the mechanisms of action.

Alveolar Bone Loss↗
PubMed1995

Periodontal disease and leucopenia.

Periodontal disease is rare in nature but widespread in domestic dog and cat populations. Unnatural diets are known to facilitate the buildup of oral microbial communities which then interact with host-immune defences giving rise to periodontitis. Eight of 14 animals undergoing dental treatment and dietary change at a suburban veterinary practice were investigated and found to have low leucocyte counts. Follow-up testing revealed changes averaging a 77.7 per cent increase with concomitant 'subjective good health'. These findings serve to cast doubt on the commonly used haematological reference ranges where the subject animals may have suffered from periodontal disease. The demonstrated reversibility of white cell depression associated with periodontal disease should provide a focus for further research.

Animals↗
PubMed2005

Stress and the periodontal diseases: growth responses of periodontal bacteria to Escherichia coli stress-associated autoinducer and exogenous Fe.

Psychological stress is known to increase the circulating levels of the catecholamine hormones noradrenaline and adrenaline, which have been shown to influence the growth of a large number of bacterial species by acting in a siderophore-like manner or by inducing the production of novel autoinducers of growth. As we have previously demonstrated that periodontal organisms display differing growth responses to noradrenaline and adrenaline, the aim of this study was to determine whether these growth effects were based upon either siderophore-like or autoinducer mechanisms. Initial inocula of 43 microbial organisms normally found within the subgingival biofilm were established under anaerobic conditions (35 degrees C). Each strain was re-inoculated into a serum-based minimal medium and growth was assessed by optical density (OD(600 nm)) with test and control cultures performed in triplicate. Test cultures were supplemented with either 50 mum ferric nitrate or a previously described Escherichia coli autoinducer of growth. Significant growth effects for supplementation with ferric nitrate (13 species responding positively) and E. coli autoinducer (24 species responding positively) were observed, with differences in growth response within bacterial species and within microbial complexes. When data for all organisms were compared with published responses to catecholamines there were only weak correlations with Fe (r = 0.28) and E. coli autoinducer (r = 0.34) responses. However, large positive responses (> 25% increase) to free Fe and/or E. coli autoinducer were significantly more prevalent in the group of organisms (n = 12) known to exhibit similar responses to catecholamine hormones (P < 0.01; chi2 = 4.56). The results support the view that catecholamines may exert their effects on subgingival organisms by initiating autoinducer production, or simply by acting in a siderophore-like manner, scavenging bound iron from the local environment. It is possible that autoinducer mechanisms may play an important role in the response of oral microorganisms to stress hormones, thereby contributing to the clinical course of stress-associated periodontal diseases.

Bacteria↗