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The relationships between periodontitis and systemic disease and conditions, environmental factors, and behavioral influences are evolving rapidly. Success in preventing and treating periodontal diseases may well rest to a large extent on our understanding of the relevant influences which may exacerbate and perpetuate the disease process. As researchers work to clarify these relationships, we as practitioners must continue to alter our treatment in the best interests of the patient's overall health. The impact of recent findings on the development and progression of periodontitis relevant to diabetes mellitus, HIV, genetic susceptibility, smoking, stress, and osteoporosis is reviewed.
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PMID:Periodontitis--the risks for its development. 1119 18

Relationship between insulin-dependent diabetes mellitus complicated by periodontitis of different severity and the plasma and vascular-platelet components of hemostasis and blood rheology was studied with the aim of early diagnosis of coagulation disorders and evaluating their significance in the mechanism of thrombohemorrhagic complications. Clinical status of patients correlated with their blood clotting parameters, particularly so in severe periodontitis. For correction Bioplant was used to replace bone pouches in surgical treatment of periodontitis.
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PMID:[Status of the hemostasis system in periodontitis in patients with insulin-dependent diabetes mellitus as criteria of disease severity and treatment efficacy]. 1123 55

It has been assumed that there is a relationship between periodontal diseases and diabetes mellitus, however the putative periodontal microorganisms in non-diabetes mellitus (non-DM) individuals and non-insulin-dependent diabetes mellitus (NIDDM) patients have not been well studied. In this study, the detection rates of 5 putative periodontal pathogens: Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Eikenella corrodens, Treponema denticola, and Candida albicans by polymerase chain reaction (PCR) between NIDDM and non-DM adults were compared. A total of 246 adults were randomly recruited and periodontal parameters including: plaque index (P1I), gingival index (GI), probing depth (PD) and attachment level (AL) were recorded. Subgingival plaque samples were collected by sterile curettes from the most diseased and healthy sites based on PD and AL. The differences in periodontal parameters and microbiological data in healthy and diseased sites between non-DM and NIDDM patients were compared by chi-square analysis. The results showed no significant differences in age, gender, GI, P1I, PD, and prevalence of the 5 microorganisms between the NIDDM and the non-diabetic groups. However, except for A. actinomycetemcomitans, the prevalence of the periodontal microorganisms tested was significantly higher (p <0.001) in diseased sites than in the healthy sites in both groups. The P1I, GI, PD and AL were significantly higher in T. denticola positive sites than in negative sites. The results suggested that P. gingivalis, T. denticola, E. corrodens and C. albicans may play important roles in the periodontitis of both NIDDM and non-DM individuals, however the etiology of periodontitis in both groups may not be different from each other.
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PMID:Detection of putative periodontal pathogens in non-insulin-dependent diabetes mellitus and non-diabetes mellitus by polymerase chain reaction. 1124

Periodontitis is a chronic inflammatory disease of the tooth supporting tissues which has a prevalence of 35% in the adult population. Risk factors are dental plaque, calculus, smoking, diabetes mellitus, stress and genetic traits. In parallel with chronic intestinal inflammatory diseases and stomach cancer, gene polymorphisms in the interleukin-I gene family are associated with severity of periodontitis. Periodontitis is usually painless. Symptoms of the disease are bleeding, redness and swelling of the gums, suppuration and migration of teeth. Halitosis may be present. Treatment of periodontitis involves supra- and subgingival mechanical debridement, oral hygiene instruction and surgical elimination of residual deepened and bleeding pockets on indication. Microbiological testing can be used to select patients who may benefit from additional systemic antimicrobial therapy. Periodontal lesions may act as a portal of entry for dissemination of periodontal bacteria into the blood stream, which may result in extraoral infections. For this reason it is recommended to include diagnosis of periodontitis in focal examination. Associations have been documented between periodontitis and cardiovascular diseases, arthritis and premature low birth weight infants.
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PMID:[Periodontitis: a hidden chronic infection]. 1129 93

Specific bacteria cause periodontitis by activating immuno-inflammatory responses in the tissues. There are certain risk factors that significantly affect the disease process by altering the immuno-inflammatory response and increasing the likelihood of severe periodontitis. These risk factors are smoking, diabetes, IL-1 genotype, and perhaps others. Today about 20 percent of the population smokes at a level that should make a difference relative to periodontitis. About 30 to 33 percent of the Caucasian population is IL-1 genotype positive. There are compelling reasons to look at these risk factors in your practice to help formulate a complete treatment plan for your patients.
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PMID:Is periodontitis genetic? The answer may be Yes! 1132 54

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.
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PMID:Periodontal manifestations of systemic disease. 1135 36

The purpose of this study was to investigate the associations between gingival crevicular fluid (GCF) elastase levels, clinical measures of periodontal status, and metabolic control of diabetes in insulin dependent (type 1) diabetes (IDDM) and non-insulin dependent (type 2) diabetes (NIDDM) patients. Sixty patients were recruited from the Diabetes Center at the University of California in San Francisco. Thirty subjects were type 1 diabetics and 30 subjects were type 2 diabetics. Metabolic control was evaluated by glycosylatted hemoglobin (HbA1c) levels. Demographic information was obtained using a structured interview with the subjects. Clinical measurements and GCF samples were taken from the mesio-buccal surfaces of 2 premolars and 2 molars from the most diseased sextant. GCF elastase was determined by measurement of p-Nitroanalide resulting from hydrolysis of elastase specific peptide. Crevicular fluid elastase levels were significantly correlated with gingival index, bleeding index, probing depth and attachment level in both type 1 and type 2 diabetes groups (0.01 <p < 0.001). HbA1c levels were not correlated with clinical measurements and GCF elastase. The results suggest that GCF elastase. age and smoking are risk indicators for periodontitis in patients with diabetes mellitus, and periodontal status is not associated with the duration and metabolic control of diabetes.
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PMID:Crevicular fluid elastase levels in relation to periodontitis and metabolic control of diabetes. 1145 15

Histamine is a classical, but still interesting inflammatory mediator. Many people have long believed that histamine is derived from mast cells or basophils alone. However, the histamine-forming enzyme, histidine decarboxylase (HDC), is induced in a variety of tissues in response (i) to gram-positive and gram-negative bacterial components (lipopolysaccharides, peptidoglycan, and enterotoxin A) and (ii) to various cytokines (IL-1, IL-3, IL-12, IL-18, TNF, G-CSF, and GM-CSF). HDC is induced even in mast-cell-deficient mice. The histamine newly formed via the induction of HDC is released immediately and may be involved in a variety of immune responses. Reviewing our work and that of Schayer and Kahlson, the pioneers in this field, lead us to the conclusion that nowadays we need to understand that histamine can be produced via the induction of HDC by a mechanism coupled with the cytokine network. We call this histamine "neohistamine", to distinguish it from the classical histamine derived from mast cells or basophils. Neohistamine is involved in physiological reactions, inflammation, immune responses and a variety of diseases such as periodontitis, muscle fatigue (or temporomandibular disorders), stress- or drug-induced gastric ulcers, rheumatoid arthritis, complications in diabetes, hepatitis, allograft rejection, allergic reactions, tumor growth, and inflammatory side effects of aminobisphosphonates.
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PMID:[Induction of histidine decarboxylase in inflammation and immune responses]. 1149 27

In the 1960s and 1970s, data became available indicating that most of the adult population had periodontal disease and that effective bacterial removal prevented and treated periodontitis. This information led to a systematic approach to the management of periodontal disease and influenced teaching of periodontics in dental schools. We now know that most adults have only gingivitis and very mild localized periodontitis. A small percentage, albeit representing substantial numbers, of adults have generalized severe periodontitis. We also recognize that a few currently known and measurable risk factors, including diabetes, smoking, and genetics, can identify the patients who are at risk for the severe generalized cases that require extensive therapy and intensive prevention, as well as patients at risk for a less-predictable response to treatment. This review will discuss the evidence that supports the change in our knowledge and understanding of periodontal disease. The question now becomes at what point, and how, do we integrate this new knowledge into the dental curriculum?
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PMID:Patients are not equally susceptible to periodontitis: does this change dental practice and the dental curriculum? 1151 50

Diabetes mellitus consists of a group of disorders, which are characterized by a lack of insulin production or insulin resistance. There can be various oral manifestations of diabetes, such as xerostomia and an increased incidence of dental caries. Recently, it has been suggested that periodontitis be added as the sixth complication of diabetes mellitus. It has been shown that uncontrolled or poorly controlled diabetics have a greater incidence of severe periodontal disease compared with those patients who are well controlled or have no diabetes mellitus. This has been found for both type 1 and type 2 diabetics. In addition, the diabetic patient may be predisposed to periodontal disease based on the production of advanced glycation end products, which bind to receptors on specific cells such as the monocyte. The success of periodontal treatment appears to be dependent on the control exhibited by the diabetic patient. The well-controlled diabetic will respond well to periodontal treatment, while the uncontrolled or poorly controlled will often not respond well or be stable in the long-term. Because of the large number of diabetics in the US population, dental therapists should be aware of the interactions of the patient's diabetic status, the proposed treatment, and the possible treatment outcomes as well as complications.
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PMID:Diabetes mellitus: a review of the literature and dental implications. 1169 99


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