Periodontal disease is a chronic inflammatory condition characterized by destruction of the periodontal tissues and resulting in loss of connective tissue attachment, loss of alveolar bone, and the formation of pathological pockets around the diseased teeth. Some level of periodontal disease has been found in most populations studied and is responsible for a substantial portion of the tooth loss in adulthood.

Periodontal Disease: The sixth complication of diabetes mellitus

Specific risk indicators associated with either susceptibility or resistance to severe forms of periodontal disease were evaluated in a cross-section of 1,426 subjects, 25 to 74 years of age, mostly metropolitan dwellers, residing in Erie County, New York, and surrounding areas. The study sample exhibited a wide range of periodontal disease experience defined by different levels of attachment loss. Therefore, it was possible to accurately assess associations between the extent of periodontal disease and patient characteristics including age, smoking, systemic diseases, exposure to occupational hazards, and subgingival microbial flora. Age was the factor most strongly associated with attachment loss, with odds ratios for subjects 35 to 44 years old ranging from 1.72 (95% CI: 1.18 to 2.49) to 9.01 (5.86 to 13.89) for subjects 65 to 74 years old. Diabetes mellitus was the only systemic disease positively associated with attachment loss with an odds ratio of 2.32 (95% CI: 1.17–4.60). Smoking had relative risk...

Assessment of risk for periodontal disease. I. Risk indicators for attachment loss.

Periodontitis is a common chronic inflammatory disease characterised by destruction of the supporting structures of the teeth (the periodontal ligament and alveolar bone). It is highly prevalent (severe periodontitis affects 10–15% of adults) and has multiple negative impacts on quality of life. Epidemiological data confirm that diabetes is a major risk factor for periodontitis; susceptibility to periodontitis is increased by approximately threefold in people with diabetes. There is a clear relationship between degree of hyperglycaemia and severity of periodontitis. The mechanisms that underpin the links between these two conditions are not completely understood, but involve aspects of immune functioning, neutrophil activity, and cytokine biology. There is emerging evidence to support the existence of a two-way relationship between diabetes and periodontitis, with diabetes increasing the risk for periodontitis, and periodontal inflammation negatively affecting glycaemic control. Incidences of macroalbuminuria and end-stage renal disease are increased twofold and threefold, respectively, in diabetic individuals who also have severe periodontitis compared to diabetic individuals without severe periodontitis. Furthermore, the risk of cardiorenal mortality (ischaemic heart disease and diabetic nephropathy combined) is three times higher in diabetic people with severe periodontitis than in diabetic people without severe periodontitis. Treatment of periodontitis is associated with HbA1c reductions of approximately 0.4%. Oral and periodontal health should be promoted as integral components of diabetes management.

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Periodontitis and diabetes: a two-way relationship

Known risk factors for coronary heart disease do not explain all of the clinical and epidemiological features of the disease. To examine the role of chronic bacterial infections as risk factors for the disease the association between poor dental health and acute myocardial infarction was investigated in two separate case-control studies of a total of 100 patients with acute myocardial infarction and 102 controls selected from the community at random. Dental health was graded by using two indexes, one of which was assessed blind. Based on these indexes dental health was significantly worse in patients with acute myocardial infarction than in controls. The association remained valid after adjustment for age, social class, smoking, serum lipid concentrations, and the presence of diabetes. Further prospective studies are required in different populations to confirm the association and to elucidate its nature.

https://www.bmj.com/content/bmj/298/6676/779.full.pdf

Association between dental health and acute myocardial infarction.

Recent evidence implicates Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis. This paper reviews the morphological, biochemical and serological charcteristics of A. actinomycetemcomitans, evidence incriminating it as a periodontopathogen, its importance in human nonoral infections, and virulence factors which may be involved in the pathogenesis of A. actinomycetemcomitans infections. A. actinomycetemcomitans is a non-motile, gram-negative, capnophilic, fermentative coccobacillus which closely resembles several Haemophilus species but which does not require X or V growth factors. The organism has been categorized into 10 biotypes based on the variable fermentation of dextrin, maltose, mannitol, and xylose and into 3 serotypes on the basis of heat stable, cell surface antigens. A. actinomycetemcomitans' primary human ecologic niche is the oral cavity. It is found in dental plaque, in periodontal pockets, and buccal mucosa in up to 36% of the normal population. The organism can apparently seed from these sites to cause severe infections throughout the human body such as brain abscesses and endocarditis. There is a large body of evidence which implicates A. actinomycetemcomitans as an important micro-organism in the etiology of localized juvenile periodontitis including: (1) an increased prevalence of the organism in almost all localized juvenile periodontitis patients and their families compared to other patient groups; (2) the observation that localized juvenile periodontitis patients exhibit elevated antibody levels to A. actinomycetemcomitans in serum, saliva and gingival crevicular fluid; (3) the finding that localized juvenile periodontitis can be successfully treated by eliminating A. actinomycetemcomitans from periodontal pockets; (4) histopathologic investigations showing that A. actinomycetemcomitans invades the gingival connective tissue in localized juvenile periodontitis lesions; (5) the demonstration of several pathogenic products from A. actinomycetemcomitans including factors which may: (a) facilitate its adherence to mucosal surfaces such as capsular polysaccharides; (b) inhibit host defense mechanisms including leukotoxin, a polymorphonuclear leukocyte chemotaxis inhibiting factor, and a lymphocyte suppressing factor (c) cause tissue destruction such as lipopolysaccharide endotoxin, a bone resorption-inducing toxin, acid and alkaline phosphatases, collagenase, a fibroblast inhibiting factor and an epitheliotoxin.(ABSTRACT TRUNCATED AT 400 WORDS)

Actinobacillus actinomycetemcomitans in human periodontal disease

Because infections and inflammatory reactions often increase the insulin requirements of previously stable patients who have diabetes, this study of periodontal infections in young patients with insulin-dependent diabetes mellitus was undertaken.

https://jada.ada.org/article/S0002-8177(82)45042-6/pdf

Prevalence of Periodontal Disease in Insulin-Dependent Diabetes Mellitus (Juvenile Diabetes)

Polymorphonuclear leukocyte (PMNL) chemotaxis studies of 32 patients with localized juvenile periodontitis (periodontosis or LJP), 10 adult patients with a history of LJP (post-LJP), 8 patients with generalized juvenile periodontitis (GJP), and 23 adults with moderate to severe periodontitis were performed: (i) to determine the prevalence of a PMNL chemotaxis defect in a large group of LJP patients; (ii) to study PMNL chemotaxis in patients with other forms of severe periodontal disease; and (iii) to determine if the PMNL chemotaxis defect seen in LJP patients is a cell-associated defect or is mediated by humoral factors. The effect of periodontal treatment on PMNL chemotaxis was studied in nine LJP patients. The chemotactic response was measured with the Boyden chamber procedure, and patient's peripheral PMNL were compared with those of control subjects, using endotoxin-activated serum, bacterial factor, N-formylmethionyl-leucylphenylalanine, and leukocyte-derived chemotactic factor as the standard chemoattractants. Based upon statistical analysis of chemotaxis assays, most carried out on at least two and often three or more separate occasions, 26 of 32 LJP patients, 7 of 10 post-LJP patients, and 5 of 8 GJP patients exhibited cellular defects of chemotaxis, whereas only 2 of 23 of the patients with adult periodontitis exhibited depressed chemotaxis. Elevated PMNL chemotaxis was occasionally found in subjects with juvenile periodontitis (2 of 32 with LJP and two of eight with GJP); however, it was found in a significant number (10 of 23) of patients with adult periodontitis. In eight of nine LJP patients, depressed PMNL chemotaxis was observed before and after periodontal therapy. The results indicate that the PMNL chemotaxis defect observed in juvenile periodontitis is due to a cell-associated defect of long duration. These studies suggest that the PMNL plays a major protective role against periodontal infection and that the cellular chemotactic defects and may predispose subjects to LJP.

https://iai.asm.org/content/iai/27/1/124.full.pdf

Neutrophil chemotaxis dysfunction in human periodontitis.

Localized juvenile periodontitis (LJP) is characterized by severe, early onset alveolar bone loss, localized to the first molars and incisors and a high prevalence of infection with Actinobacillus actinomycetemcomitans and associated neutrophil functional abnormalities Due to the frequent occurrence of this condition in families, it was the purpose of this investigation to determine the association of neutrophil chemotaxis abnormalities and clinical periodontal disease in families with LJP Twenty-two families were studied in which the proband was selected based upon presentation of LJP All siblings were examined for the presence of LJP and neutrophil chemotaxis was measured on all subjects The results indicate that there is a high association of LJP and neutrophil chemotaxis disorders and that this association is consistent along family lines Specially, in families in which the proband exhibits a neutrophil chemotaxis disorder, all affected siblings (LJP) also exhibit depressed neutrophil chemotaxis, whereas, non-affected siblings beyond the age of puberty have normal neutrophil chemotaxis On the other hand, in families where the proband (LJP) exhibits normal chemotaxis, both normal and affected siblings exhibit normal chemotaxis The finding among families with LJP that some exhibit neutrophil chemotactic depression and others exhibit normal neutrophils suggests heterogeneity of LJP Accordingly, it is proposed that there is a syndrome of familial localized juvenile periodontitis with depressed neutrophil chemotaxis and another form of familial localized juvenile periodontitis with normal neutrophil chemotaxis The chemotaxis disorder and LJP occur in nearly one-half of the siblings in families with LJP which is consistent with a dominant trait however, multigenerational studies are necessary to determine the mode of inheritance Hence, neutrophil chemotaxis is a disease marker which can be used in genetic studies of familial LJP with depressed neutrophil chemotaxis Furthermore, prepubertal siblings often exhibit defective neutrophil chemotaxis in the families in which the proband exhibits such a defect Since the prepubertal siblings are not affected by clinically detectable LJP, the finding of neutrophil chemotactic depression in these children further suggests that the neutrophil chemotactic defect is genetic in origin, precedes and may predispose to localized juvenile periodontitis

L. J. Cianciola

Papers

Prevalence of Periodontal Disease in Insulin-Dependent Diabetes Mellitus (Juvenile Diabetes)

Neutrophil chemotaxis dysfunction in human periodontitis.

Neutrophil chemotaxis in families with localized juvenile periodontitis.

Relationship of the neutrophil to host resistance in periodontal disease.