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PubMed2006

[Links between periodontal disease and general health. 2. Preterm birth, diabetes and autoimmune diseases].

The condition of the periodontium may effect people's general health. There is evidence of a correlation between periodontal disease and preterm birth or low birth weight. In pregnant women with periodontal disease, scaling and root planing seems to reduce the risk of preterm birth or low birth weight. Furthermore, periodontal disease appears to have an adverse effect on glycemic control in diabetics. However, periodontal treatment as a means to glycemic control is restricted unless it includes the use of systemic antibiotics. Slowly, a possible correlation between periodontal disease and autoimmune diseases is emerging. Further research into the correlations between periodontal disease and systemic health is desirable and might well result in new therapeutic options.

Autoimmune Diseases↗
PubMed1998

Effect of estrogen supplementation on periodontal disease.

This article presents evidence of the protective role of estrogen supplementation on periodontal disease in postmenopausal women. A total of 412 women, 236 postmenopausal (50 to 75 years old) and 176 premenopausal (25 to 49 years old), were included in this study. The postmenopausal group included 59 women receiving estrogen replacement therapy (ERT) and 177 who did not receive ERT (non-ERT). Periodontal disease was assessed from two independent but highly correlated measures: clinical attachment loss (CAL) and alveolar bone loss (ABL). Severe periodontal disease was arbitrarily defined as mean CAL or ABL > or = 3 mm. Data adjusted for age effect were compared for various groups of premenopausal and postmenopausal women. Non-ERT women were twice as likely as their ERT counterparts, and three times more likely than premenopausal women, to exhibit severe attachment loss. Individual percentages of women affected by severe attachment loss were 18.6%, 11.9%, and 6.3% for non-ERT, ERT, and premenopausal women, respectively. On the other hand, severe ABL was detected in 34%, 20.3%, and 9.7% of the non-ERT, postmenopausal ERT, and premenopausal women, respectively. Similar to CAL, when ABL was used as a measure of disease, almost twice as many non-ERT women compared to their ERT counterparts and four times compared to premenopausal women exhibited severe ABL. Therefore, ERT appears to have a protective effect on the severity of periodontal disease and the periodontium.

Adult↗
PubMed1984

Host responses in periodontal diseases.

Great progress has been made in our understanding of the pathogenesis of periodontal disease, the primary role of bacteria as etiologic agents, and the critical modifying role of host responses. It is useful to consider several stages in the pathogenesis of periodontal disease - (a) colonization, (b) invasion, (c) destruction, and (d) healing - and to place into perspective the various host responses as they may affect each of these four stages (Table 5). With respect to colonization, although very little direct evidence is available, it is reasonable to suggest that antibodies, either secretory or serum-derived, acting by virtue of their ability to block attachment, could inhibit colonization by immune reduction of adherence mechanisms. With respect to invasion of the tissue, it appears that phagocytes, particularly the neutrophils, are important, acting in concert with opsonic antibody and complement in ingesting and killing the periodontal microflora before or during the early invasive process. A major advance in our understanding of the pathogenesis of periodontal diseases is the realization that the virulence of periodontopathic bacteria relates to their leukaggressive properties, allowing them to evade neutrophil protective mechanisms. Invasion of the periodontal tissues by bacterial products may be inhibited by the complexing of these products with antibody with the formation of antigen-antibody complexes that are phagocytosed and digested, particularly by scavenger phagocytes such as the macrophage. With respect to the destructive phase of periodontal disease, it is clear that the direct effect of lymphocytes mediated either through direct cytotoxic activity, or through biologically-active destructive lymphokines (such as alpha-lymphotoxin and osteoclast activating factor), can lead to tissue destruction. Macrophages, through the production of monokines, collagenase, and reactive oxygen species, can also lead to tissue destruction. The direct effects of bacterial toxins or enzymes which can lead to tissue destruction can be inhibited by complexing with antitoxic or enzyme-neutralizing antibodies. With respect to healing and fibrosis, very little direct information is available; however, it is possible that the lymphocytes and macrophages affect fibrosis by the production of chemotactic factors for fibroblasts which would be expected to bring them to the area of periodontal inflammation and also by production of fibroblast-activating factors, which then cause the fibroblasts to proliferate and produce collagen which replaces lost collagen or results in fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Aggressive Periodontitis↗
PubMed1991

Prosthetic reconstruction of dentitions seriously compromised by periodontal disease.

Dentitions seriously compromised by periodontal disease are often in need not only of cause-related periodontal therapy of high quality but also of relevant prosthetic rehabilitation. Contrary to traditional claims, clinical investigations published during the last 2 decades demonstrate that, if adequately treated and controlled, such dentitions can carry fixed, cross-arch bridges on an extremely reduced amount of periodontium, with a good long-range prognosis. It has also been shown that a markedly reduced but healthy and favourably distributed periodontium supporting such constructions can withstand occlusal forces of considerable magnitude. Another controversial topic, related to fixed bridges, involves indications and contra-indications for cantilever segments. Some clinical investigations demonstrate a markedly increased risk of failure if the fixed bridge is provided with cantilever units, while other controlled studies with defined specifications on the design of the constructions exhibit a high success rate after 8 years or more also for bridgework where 2 or 3 cantilever units are included. The force pattern along cantilever segments of both tooth-supported and implant-supported bridges has been extensively studied. The results show that the force distribution depends not only on the occlusal contact pattern and the dimensioning of the cantilever beam, but also on the type of prosthetic construction in the opposite jaw occluding with the cantilever segment. The free-standing, implant-supported bridge has recently become an important treatment modality for rehabilitation of the partially edentulous jaw, and follow-up studies demonstrate a high success rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Denture Design↗
PubMed1989

Cigarette smoking as risk factor in chronic periodontal disease.

Patients admitted to the School of Dentistry, Stockholm, for treatment of chronic periodontal disease during the years 1980-82 were retrospectively investigated with respect to their smoking habits. The investigation was designed as a case control study and covered all patients 30, 40, or 50 yr of age upon admission, in all 155. As control served a random sample of the Stockholm population. The periodontal variables under scrutiny were frequency of periodontally diseased teeth, frequency of periodontally diseased sites (probing depth greater than 4 mm), gingival index, and plaque index. The overall occurrence rate of smokers in the sample of cases was 56%, which is significantly greater than the population at large. This held true for all three age cohorts and for men as well as women. The risk ratio was 2.5, indicating more prevalent disease among smokers. Further, significantly greater frequencies of periodontally involved teeth and diseased sites were found in smokers, indicating more severe disease among smokers. Gingival index and plaque index did not notably differ between smoking groups. The results suggest increased prevalence as well as severity in smokers. Smoking, therefore, should be considered a risk factor for chronic periodontal disease.

Adult↗
PubMed1978

Diabetes mellitus and periodontal disease.

A sample of 54 patients with diabetes mellitus were subjects to detailed assessment of periodontal disease levels using standard indices. In order to determine whether the severity of periodontal disease was related to the severity of diabets mellitus, a series of parameters of the diabetes mellitus population was simultaneously studied. There were no significant relationships between the levels of periodontal disease and the duration of diabetes, the type of treatment and the frequency of systemic complications. Periodontal disease in the diabetic appeared to the affected by the same etiologic factors [plaque, calculus, neglect] as would be expected in nondiabetic patients. Further studies with larger population samples would be appropriate.

Adult↗
PubMed2004

Periodontal disease and weight loss in older adults.

OBJECTIVES: To determine the association between periodontal disease and weight loss in an elderly cohort. DESIGN: A longitudinal design was used with participants from the Health, Aging and Body Composition (Health ABC) cohort study to determine the association between periodontal disease status and weight loss of at least 5% of baseline body weight over a period of 2 years. SETTING: Participants were examined in research clinics in Pittsburgh, Pennsylvania, and Memphis, Tennessee. PARTICIPANTS: A randomly selected subset of 1,053 individuals from the Health ABC examination, aged 65 and older, ambulatory and community-dwelling at baseline. MEASUREMENTS: Periodontal disease was measured as mean pocket depth and attachment loss, extent (percentage) of pockets with at least 6 mm probing depth, extent of bleeding on probing, and tissue inflammation. RESULTS: In logistic regression models adjusting for variables that may explain weight loss, extent of periodontal pockets with at least 6 mm probing depth showed a significant association with weight loss (odds ratio=1.53, 95% confidence interval=1.32-1.77). CONCLUSION: Periodontal disease may be causally related to weight loss in the elderly and thus may increase risk of morbidity and mortality.

Aged↗
PubMed1994

Periodontal disease as a risk factor for heart disease.

Many individuals with cardiovascular disease appear from epidemiologic studies to have either periodontal disease or to be edentulous. A Finnish group has provided evidence that after conventional risk factors for stroke and heart attacks have been accounted for, there still remains a significant relationship between dental disease and cardiovascular disease. A preliminary analysis of our own investigation of the interrelationship of medical and dental health shows that individuals with a high dental morbidity (ie, edentulous or with many missing teeth) have a high prevalence of coronary heart disease and stroke. A model based on how smoking can predispose to periodontal disease is used to explain how periodontal disease could be a potential risk factor for heart disease.

Bacteremia↗
PubMed1998

Pharmacologic management of periodontal diseases using systemically administered agents.

Since the establishment of bacteria-laden plaque as a causative agent in gingivitis, the search for specific bacteria that induce different types of periodontitis has generated extensive research. In contrast to many other microbial-induced disorders, the specific periodontal pathogen(s) has not been identified to date. Therefore, the search for an effective systemic agent to prevent the loss of attachment through the selective reduction of known periodontal pathogens has remained elusive. It is not surprising then that antibiotics are not used solely to manage periodontal diseases but rather as an adjunct to the mechanical débridement of root surfaces in select periodontal diseases. Further, the sole use of antibiotics in patients with adult periodontitis (or those who exhibit signs of inflammation but are periodontally stable) has shown little benefit and only increases the chance of microbial resistance to antibiotics. Despite these limitations, considerable progress in antibiotic therapy has delivered regimens that enhance the effectiveness of conventional therapy. In contrast to traditional antimicrobial therapy, new treatment modalities have begun to focus on modulating the responses of host cells to bacteria rather than modulating only the bacteria. Current drugs used to regulate host cells inhibit the cyclooxygenase pathway, reduce the activity of metalloproteinases, or inactivate bone resorptive cells (see Table 1). Although these drugs offer great potential to modulate a variety of mammalian cells, a notable and consequential limitation of these agents is a lack of specificity. Inflammation, bone metabolism, and connective tissue metabolism are two-edged swords; all are necessary for the homeostasis of the tissue, but some or all may also be involved in the pathologic destruction of that same tissue. Hence, drugs that inhibit destruction of the connective tissue in one site of the periodontium also interfere with wound healing at another. As a result of these limitations, the efficacy, safety, and cost-effectiveness of the long-term use of these agents is unknown. Preliminary results of treatment with these drugs are promising, and future generations of host-modulating drugs will provide clinicians with additional agents to help improve the success rate of periodontal treatment for patients. Antibiotics remain an important adjunctive therapy in the treatment of periodontal diseases, and the use of host modulating drugs as supplemental agents in the management of periodontal diseases continues to grow. As more knowledge is gained about the causes of periodontal diseases, new drugs that are potent, effective, site specific, and safe can be delivered at optimal times by simply having the patient take a few tablets. Considering the dramatic progress in the past decade in understanding the cause and pharmacologic management of periodontal diseases, the twenty-first century holds great promise for the development of magic bullets.

Adult↗
PubMed2007

The association between serum folate levels and periodontal disease in older adults: data from the National Health and Nutrition Examination Survey 2001/02.

OBJECTIVES: To assess the relationship between serum folate levels and periodontal disease in older adults. DESIGN: Population-based cross-sectional study. SETTING: National Health and Nutritional Examination Survey 2001/02. PARTICIPANTS: Eight hundred forty-four dentate elderly subjects aged 60 and older (mean age 70.6) who completed a periodontal examination and laboratory test for serum folate levels. MEASUREMENTS: Periodontal examination, including probing depth and attachment loss, was performed. Periodontal disease was defined as having at least 10% of sites with clinical attachment loss of more than 4 mm and at least 10% sites with probing depth of more than 3 mm. Serum folate levels were measured using a commercially available radioprotein binding assay kit. RESULTS: After controlling for demographics, educational level, body mass index, bleeding on probing, and probing sites, the odds ratio for periodontal disease was 0.74 (95% confidence interval=0.59-0.93) for each standard deviation increase in natural-log-transformed folate levels. After additionally controlling for levels of vitamin B(12) and homocysteine, chronic diseases (hypertension, diabetes mellitus, heart disease, and stroke), and health behaviors (smoking status and alcohol consumption), the negative association between folate level and periodontal disease remained statistically significant and essentially unchanged. There was no effect modification of sex on the association between serum folate levels and periodontal disease. CONCLUSION: A low serum folate level was independently associated with periodontal disease in older adults. The results suggest that serum folate levels, important indicators of periodontal disease in older adults, may provide an important clinical target for intervention to promote oral health.

Aged↗
PubMed2001

[A 10-year longitudinal study of the progression of destructive periodontal disease in adult and elderly].

OBJECTIVE: To study the progression of destructive periodontal disease in adult and elderly aged 20 to 80. The examinees were followed 10 years to determine whether the rates for progression of periodontal disease were different than the populations in the more developed countries. METHODS: In 1984, at baseline, 587 subjects had been examined and by 1994, 440 of them still available for follow-up study, and 398 persons remained dentate. Tooth mobility, plaque, calculus, gingival conditions, attachment levels, and probing depths on 4 sites of each tooth present were checked and recorded by the same two examiners. RESULTS: All subjects had > or = 2 mm attachment loss over 10-year period. Some teeth, such as mandibular incisors and maxillary molars, had higher progression rate than others. The mean attachment loss rate did not differ significantly between age groups, and were similar to those reported for populations in the more developed countries. CONCLUSIONS: The rate for progression of periodontal disease in this study were not significantly different between the examinees and the populations in more developed countries; and also were not significantly different among the different age groups. The causes of destructive periodontal disease in humans are more likely intrinsic factors.

Adult↗
PubMed2001

Hypothalamic-pituitary-adrenal axis activation by experimental periodontal disease in rats.

Organisms respond to inflammatory conditions by mounting a co-ordinated complex series of adaptive responses involving the immune, nervous and endocrine systems that are aimed at restoring the homeostatic balance. We have recently shown in a rat model that inappropriate hypothalamic-pituitary-adrenal (HPA) axis regulation and a subsequent inability to mount a suitable glucocorticoid response to gingival inflammation may influence susceptibility to periodontal disease. This study was designed to investigate whether ligature- and bacterial lipopolysaccharide (LPS)-induced inflammation in the gingival connective tissues may activate this physiological axis, and to further explore the significance of HPA regulation in periodontal disease. Experimental periodontal disease was induced in major histocompatibility complex (MHC)-identical but HPA low (LEW) and high (F344) responding rat strains. We tested (1) whether ongoing periodontal disease activates the HPA axis as measured by corticosterone levels, and (2) whether genetic differences in HPA regulation modulate periodontal disease progression. In the F344 strain. the periodontal tissue destruction was more severe. This observation was associated with a significant increase of corticosterone levels in F344 rats only. Addition of LPS at the gingival inflammatory site led to a further increase of corticosterone levels and disease severity in F344 rats. These findings illustrate a positive feedback loop between the HPA axis and periodontal disease: the disease activates the HPA axis, and a genetically determined high HPA responsivity further increases disease susceptibility.

Alveolar Bone Loss↗
PubMed1979

Prevention of periodontal disease in the future.

Existing knowledge about periodontal disease is sufficient to permit the interested individual to carry out a preventive program which can result in preventing the major forms of the disease from developing. It is likely that the sooner such a program is started in a person's lifetime, the likelier it is to succeed. With the additional knowledge obtained from current avenues of research, clinical microbiology and immunology will become applicable to the management of selected forms of periodontal disease, both for diagnostic and therapeutic purposes. Some of the information gained may help in fostering the establishment of a desirable microbial flora and in better control of potentially pathogenic strains. The implementation of an effective preventive program for periodontal and other dental diseases will vary on a regional basis depending on political, economic, social and ethical considerations.

Bacteria↗
PubMedDate not supplied

[Periodontal disease in pregnancy and low birth weight]

OBJECTIVE: Recently, it has been suggested that periodontal disease during pregnancy could have a causal relationship with low weight at birth. Our objective was to evaluate the influence of periodontal disease during pregnancy on the birth weight of newborn infants. METHODS: Mothers who gave birth to low-birth-weight infants were randomly selected (Group 1 - G1; n=13). Immediately after inclusion of each mother in group 1, the mother of the next term newborn with birth weight of > 2,500 g (Group 2 - G2; n=13) was included as control. Mothers were examined by a periodontist who was not informed of the group the child belonged to. A probe was used to measure attachment loss of the alveolar bone. The extension index (EI) and severity index (SI) of the periodontal disease were determined. RESULTS: Both groups of mothers were similar in terms of maternal age, parity, color of skin, height, nutrition, smoking, drinking, socioeconomic status, prenatal examinations, premature rupture of membranes, chorioamnionitis, bacteriuria, placenta previa, abruptio placentae, previous hypertensive disease, preeclampsia, and heart disease. The characteristics of the newborns were: birth weight - G1 = 1,804 -/+ 675 g x G2 = 3,030 -/+ 516 g; gestational age - G1 = 33 -/+ 5 weeks x G2 = 39 -/+ 2 weeks; length of stay in the neonatal intensive care unit (NICU) - G1 = 128 days x G2 = 0 days. Average EI: G1 = 89.788 -/+ 18.355 x G2 = 72.420 -/+ 20.717; p=0.033. Average SI: G1 = 1.377 -/+ 0.626 x G2 = 0.754 -/+ 0.413 (OR=18.3; CI95%: 2.5-133.3; p = 0.006). After adjustment for risk factors for low birth weight, such as smoking, maternal height, bacteriuria, and previous hypertension, the odds ratio for SI dropped to 7.2 (CI95% = 0.4-125.4; P = 0.176). CONCLUSION: The multivariate analysis indicated a marked association between periodontal disease measured by SI score and low birth weight. Our data suggested that periodontal disease during pregnancy may be a risk factor for low weight at birth.

Journal Article↗
PubMed2006

Diabetes as a risk factor for periodontal disease: current status and future considerations.

INTRODUCTION: Over the past decade, there has been an emerging interest in the interrelationship between systemic conditions and oral health. Diabetes is perhaps one of the best documented conditions that have been closely linked with periodontal disease. This paper reviews the role of diabetes as a risk factor in periodontal disease. The treatment implications in the management of periodontal disease as an integral component of diabetes care is also discussed in light of the current understanding of the pathogenesis of these 2 chronic conditions. MATERIALS AND METHODS: Epidemiological, clinical and laboratory studies examining the relationship between diabetes and periodontal diseases were selected from both medical and dental journals. RESULTS: The severity of periodontal destruction has been shown to be related to the direct and indirect effects of glycaemic control, with other factors also being implicated. Although some studies have pointed towards a bi-directional relationship between glycaemic control and periodontal health, it is still not clear if improvement in periodontal health could lead to improved metabolic control. CONCLUSION: Diabetes and periodontal disease are closely related in many ways, though the effect of periodontal disease on diabetes control remain to be determined, with larger intervention studies. In light of the increasing evidence of the relationship between diabetes and periodontal disease, management of oral health should form an integral part of diabetes management.

Anti-Infective Agents↗
PubMed1999

Vascular endothelial growth factors and progression of periodontal diseases.

BACKGROUND: Tissues become hemorrhagic and edematous coincident to periodontal diseases; however, there is little information concerning the biologic mechanisms which may produce these changes. Vascular endothelial growth factor (VEGF) is a macromolecule which enhances blood vessel growth and permeability. However, there is no information concerning gingival VEGF concentrations within normal or diseased gingiva. The purpose of this study was to assess changes in gingival concentrations of VEGF during initiation and progression of periodontal diseases and compare them to changes in the number of blood vessel profiles and concentration of recognized markers of periodontal disease severity (interleukin-6[IL-6]). METHODS: Normal (non-hemorrhagic gingiva adjacent to a < or =3 mm gingival sulcus) and inflamed gingiva (hemorrhagic gingiva adjacent to a < or =3 mm, 4 to 6 mm, or >6 mm periodontal pocket) were studied. VEGF and IL-6 concentrations were assessed by ELISA and the number of blood vessels determined by histomorphometric techniques. Data were placed into one of the following groups: < or =3 mm, normal; < or =3 mm, diseased; 4 to 6 mm, diseased; and >6 mm, diseased. These groups were compared by factorial ANOVA and Scheffe comparisons. In addition, groups were compared by simple and multiple regression and regression ANOVA to determine possible correlations between them. RESULTS: VEGF and IL-6 concentrations were significantly lower within normal than within diseased gingiva. The number of blood vessel profiles and mean IL-6 concentrations were highest in diseased tissues adjacent to >6 mm sulci and were significantly correlated with sulcular depth (P <0.001). In contrast, VEGF concentrations were highest within diseased gingiva adjacent to 4 to 6 mm periodontal pockets (P <0.001) and were not correlated with sulcular depth. CONCLUSIONS: VEGF may be a factor in initiation and progression of gingivitis to periodontitis, possibly by promoting expansion of the vascular network coincident to progression of the inflammation.

Analysis of Variance↗
PubMed2001

Prevalence and risk indicators for destructive periodontal diseases in 3 urban American minority populations.

BACKGROUND, AIMS: Destructive periodontal diseases have been reported disproportionately more prevalent and severe in African-Americans relative to other American populations. Differences in subgingival microbiota and host immune response have also been reported for African-Americans, implying that risk factors for disease progression may also differ for these populations. Since it is not clear whether these differences are truly genetic or due to confounding variables such as social economic status, we examined a series of clinical, environmental, demographic, and microbiologic features associated with periodontal disease status in a group of 185 urban minority subjects resident within the greater New York metropolitan area. METHODS: The study population consisted of 56 Asian-American, 71 African-American and 58 Hispanic subjects. Clinical data recorded included pocket depth, attachment level, gingival erythema, bleeding upon probing, suppuration, and the presence of supragingival plaque. Environmental and demographic data recorded included smoking history, years resident in the United States, whether the subject reported a private dentist and occupational status. Subgingival plaque was sampled from the mesial aspect of all teeth exclusive of third molars and the levels of 40 subgingival species enumerated using checkerboard DNA-DNA hybridization. RESULTS: The African-American group had more missing teeth, deeper periodontal pocket depth and more attachment loss than the Asian-American or Hispanic groups. However, the African-American group were less likely to report having a private dentist, had a greater proportion of smokers and a greater proportion of unskilled individuals. The profile of subgingival species differed among the three ethnic/racial groups with A. actinomycetemcomitans, N. mucosa, S. noxia and T. socranskii significantly elevated in the Asian-American group and P. micros significantly elevated in the African-American group. When subset by occupational status, numbers of missing teeth, pocket depth, attachment level and prior disease activity were all found increased in the unskilled relative to the professional group. Local factors including the mean % of sites with plaque, marginal gingival erythema, bleeding upon probing and suppuration were also elevated in the unskilled group. The microbial profile differed among the 3 occupational groups with the unskilled group having elevated numbers of species associated with destructive periodontal diseases. CONCLUSIONS: Although greater destructive periodontal disease prevalence and severity were found in the African-American group, these results suggest that environmental and demographic variables, such as occupational status, may have a greater influence on risk indicators associated with disease prevalence and progression in these populations.

Adult↗