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PubMed1993

Cross-sectional studies in periodontal disease: current status and implications for dental practice.

This paper reviews the cross-sectional national studies of periodontal disease conducted over the past 30 years. Studies included are the 1960-62 HES study (NCHS), the 1971-74 NHANES I study (NCHS), the 1981 RTI study (HRSA), and the 1985-86 Employed Adults study (NIDR). For each of these surveys, the population studied, the general sampling strategy, the periodontal measures collected, and the periodontal findings are compared in this paper. Compared with the first three studies, the NIDR 1985-86 findings appear markedly lower, implying that there has been a decline in the prevalence of periodontal disease. Two possible inferences from these studies are that: (1) there has been a decline in the prevalence of periodontal disease in recent years or (2) the sampling and measurement methods may be sufficiently different for these lower numbers to result. Each inference is explored, with the authors concluding that the latter is more plausible. The implications for future treatment needs are then estimated, given the marked trends in the size of the aging population. The number of older adults over age 55 who will need periodontal services will increase. The adequacy of the number, type, and distribution of dental care providers to meet these increasing needs is discussed.

Adult↗
PubMed1995

Energy intake, dental caries and periodontal disease in 11-year-old black children in two regions of Southern Africa: KwaZulu and Namibia.

The study examined energy intake in relation to dental caries and periodontal disease in 11-yr-old rural and urban black children in low fluoride areas of KwaZulu and Namibia (0.15 ppm F) and one higher fluoride area of Namibia (1.56 ppm F). Twenty-four hour dietary recalls were conducted by trained interviewers and daily energy intake estimated using the MRC dietary analysis programme. DMFS was recorded according to WHO criteria: periodontal disease was measured using CPITN and SAS was used for statistical analysis. The prevalence of dental caries and periodontal disease (using CPITN), were compared within three energy groupings; < or = 850 kcal/day; > 850, < 1400 kcal/day and > or = 1400 kcal/day. The rural low fluoride Namibian children had the lowest mean energy intake (616 kcal/day), which also was the grouping with highest healthy periodontal prevalence (65%). The urban groups had higher energy intakes than the rural communities. Statistically significant effects on caries prevalence were seen for country and fluoride grouping; for periodontal disease, significant effects were noted for country, fluoride group and environment. Energy intake had no statistically significant effect, so this is not a risk marker for the disease.

Black or African American↗
PubMed1989

Prevalence of chronic periodontal disease using probing depth as a diagnostic test.

The prevalence of chronic periodontal disease was investigated using the occurrence of diseased pocket sites as the diagnostic criterion. The study group comprised 250 dentally aware subjects aged 21-60 years, with a high number of teeth remaining in all age groups. The % of sites with a probing depth of greater than or equal to 4 mm was 16% for the total sample. Most diseased sites (69%) were in the 4-mm class, with only 4% at depths greater than or equal to 7 mm. 82% on the subjects had 1 or more sites greater than or equal to 4 mm. With probing depth as the sole criterion for diagnosis of chronic periodontal disease, prevalence in a sample is heavily dependent on the critical levels selected for probing depth and cut-off point. With critical levels of 4 mm for probing depth and 1 diseased site for the cutoff point, prevalence was 49% in the 21-30 year age group and 95% in the 51-60 year age group. A shift in cutoff point to 40 diseased sites gave a prevalence of 2% and 41%, respectively, in the 2 age groups. For a critical depth of 7 mm and a cutoff point of 1 diseased site, the prevalence was 2% and 43% for the 2 age groups, respectively. Aspects of importance for the decision-making process on disease are discussed.

Adult↗
PubMed2006

Periodontal disease and control of diabetes mellitus.

Data from the Centers for Disease Control and Prevention indicate that more than 20 million people (approximately 7% of the population) in the United States have diabetes mellitus. Physicians often fail to examine the mouths and teeth of their patients, even though the condition of the mouth and teeth have clinical relevance for the treatment of patients with diabetes mellitus. The authors examine the current state of knowledge regarding periodontal disease and the effect of periodontal disease on worsening of glycemic control. They review several studies investigating how the management of periodontal disease affects the ability of patients to control symptoms of diabetes mellitus. The authors conclude with several recommendations for the treatment of patients with periodontal disease to improve glycemic control.

Anti-Bacterial Agents↗
PubMed1998

Is estrogen deficiency a risk factor for periodontal disease?

In recent years, interest in the relationship between osteopenia, osteoporosis, estrogen status, and periodontal disease has grown considerably. A substantial number of studies have attempted to address this important question. Despite the large body of evidence, controversy persists concerning a possible association between these conditions. Whether loss of oral bone is related to loss of systemic bone and whether estrogen deficiency modulates loss of oral bone are subjects of more specific debate. This article reviews the direct and indirect scientific evidence supporting the role of estrogen deficiency as a risk factor for periodontal disease. A model is proposed for the biological basis of such increased risk. The article also suggests essential criteria for the design of studies examining the relationship between osteopenia, osteoporosis, estrogen deficiency, and periodontal disease.

Alveolar Bone Loss↗
PubMed2005

CXCL12 and CXCR4 expression by human gingival fibroblasts in periodontal disease.

CXCL12 is a CXC chemokine that is related to lymphocyte infiltration and angiogenesis in inflammatory sites such as arthritis. However, the expression and roles of CXCL12 in periodontal disease are uncertain. The aim of this study was to assess the expression of CXCL12 and its receptor, CXCR4, in periodontal tissue and to investigate the properties of CXCL12 and CXCR4 expression by human gingival fibroblasts (HGF). RT-PCR analysis revealed that CXCL12 and CXCR4 mRNA were expressed in both normal gingival tissues and periodontal diseased tissues. Immunohistochemistry disclosed that CXCL12 was expressed and CXCR4 positive cells were found in both normal and periodontal diseased gingival tissues. Our in vitro experiments elucidated that HGF constitutively produced CXCL12, and the levels were enhanced by stimulation with tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), regulated upon activation normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein 3(alpha) (MIP-3(alpha)). On the other hand, heat killed Porphyromonas gingivalis (P. gingivalis) and P. gingivalis LPS reduced the CXCL12 production by HGF. Flow cytometry analysis clarified that CXCR4 was highly expressed on HGF, and CXCR4 expression was abrogated by TNF-alpha, IFN-gamma and P. gingivalis LPS. Moreover, CXCL12 induced vascular endothelial growth factor (VEGF) production by HGF. Our results demonstrated that CXCL12 might be related to CXCR4+ cells infiltration and angiogenesis both in normal periodontal tissues and periodontal diseased tissue. P. gingivalis, a known periodontal pathogen, inhibits the production of CXCL12 and the expression of CXCR4 by HGF. This fact means that P. gingivalis may inhibit CXCR4+ cells infiltration and neovascularization in periodontal tissue and escape from the immune response.

Cells, Cultured↗
PubMed1991

Bacteriologic monitoring of periodontal diseases: cultural, enzymatic, immunologic, and nucleic acid studies.

Evidence supporting the bacteriologic etiology of periodontal diseases has led investigators to monitor the microbiologic species associated with each disease. The type of study performed has evolved at different levels over the years and is predominantly influenced by available technologies. As the technology has advanced, so too have attempts at monitoring specific microorganisms. The ultimate goal in most research efforts on clinical bacteriologic monitoring of the periodontal diseases has been to obtain a method of measuring microorganisms in a specific, rapid, low-cost fashion. The method would be used on a daily basis at chairside in the dental operatory to direct treatment at a target microbial population, evaluate treatment, or predict future areas of attachment loss. It is suggested that future efforts try to incorporate microbiologic-host interactions that are likely to be important in the etiology and pathogenesis of the periodontal diseases.

Aggregatibacter actinomycetemcomitans↗
PubMed1992

Host mediators in gingival crevicular fluid: implications for the pathogenesis of periodontal disease.

During the past few years, a considerable number of studies have examined different aspects of the host response in gingival crevicular fluid (GCF), including the relationship of specific markers to the active phases of periodontal disease. Various indicators of the acute inflammatory response (the lysosomal enzymes beta-glucuronidase and collagenase, the cytoplasmic enzyme aspartate aminotransferase, and the arachidonic acid metabolite PGE2) have been shown to be associated with clinical attachment loss in chronic adult periodontitis in man and experimental periodontitis in animal models. In contrast, the relationship of indicators of the humoral immune response in GCF to active periodontal disease is equivocal. Furthermore, a number of indicators of the cellular immune response have been identified recently in GCF (i.e., Interleukin-1 alpha, IL-1 beta, tumor necrosis factor-alpha), but their relationship to active phases of periodontal disease have not been studied. The polymorphonuclear leukocyte (PMN) is the cellular hallmark of acute inflammation. Evidence from the GCF studies suggests that hyperreactivity of these cells plays a critical role in the active phases of some forms of periodontal disease. Metabolic activation of PMN can be associated with a number of potentially destructive reactions. The major effector mechanism for tissue destruction that can be specifically identified with the PMN is the synergistic effect of the release of PMN proteases and the generation of reactive oxygen metabolites by these cells. Priming of the PMN, where the PMN response is enhanced by agents that do not initiate the response, may be an important mechanism for PMN activation in the crevicular environment; for example, cytokines such as IL-1 beta and TNF-alpha, and lipopolysaccharides released from subgingival Gram-negative bacteria, can serve this function. The hypothesis proposed here argues that in addition to the severe forms of periodontal disease that have been associated with qualitative or quantitative PMN defects, tissue destruction in the periodontum can be observed with hyperreactivity of these cells. These differing conclusions do not create a dilemma, but may represent opposite ends of a balance that is no longer in equilibrium.

Animals↗
PubMed2001

Prevalence assessment of periodontal disease in 3-6 year old children through PSR--a pilot study.

Increasing amounts of information emphasise the relevance of prevention, early diagnosis and early treatment of periodontal diseases in children. Children and adolescents affected by periodontal disease, mainly those who present a fast and severe attachment loss, are considered to be at risk of developing early or advanced periodontitis. Alternatively they may be presenting a reflex of systemic conditions affecting the periodontium. This study was aimed at verifying the acceptability of the use of the Simplified PSR (Periodontal Screening and Recording) Index in a very young population since a previous study in Bahia, Brazil, indicated a very high need for periodontal treatment in adolescents and young adults. A total of 200 children aged 3-6 years from private schools in Bahia, Brazil, were examined by four trained undergraduate students. The screening system was well accepted by the subjects and the fact that it is a fast tool was considered important for the successful examination of all sextants without behavioural disturbance. A high prevalence and a low severity of parameters related to periodontal disease were found in this population. A statistically higher prevalence of PSR code 2 (61.5%) [54.50-68.49] CI 95% when compared to PSR codes 0 (23.5%) 117.93-30.10] CI 95%, 1 (14.5%) 110.07-20.32] CI 95% and 3 (0.5%) 10.02-3.18] CI 95% were shown. There was no statistically significant difference between female and male children for any PSR code. The finding of more parameters related to periodontal health in S5 when compared to sextants S6 and S4 showed statistical significance (CI 95%).

Brazil↗
PubMed1991

Mast cells in periodontal disease.

Since the roles of mast cells in periodontal tissues are not clear, this study aimed to count the number of mast cells in gingival tissues of healthy volunteers and patients with chronic periodontal disease before and three weeks after surgical treatment. The numbers of mast cells were found to be increased on postoperative healed tissues and inflamed tissues respectively, compared to healthy tissues. This increase is closely related to fibrosis in connective tissues.

Adult↗
PubMed1985

Inhibitory effect of periodontally diseased root extracts on the growth of human gingival fibroblasts.

Cementum shavings obtained from periodontally diseased and nondiseased areas of 100 removed, single-rooted teeth were extracted with either pyrogen-free water (PFW) for 5 minutes, 1 M citric acid for 5 minutes or 45% phenol-PFW for 90 minutes at 65 degrees C. The extracts were membrane-filtered, dialyzed exhaustively versus PFW, lyophilized, weighed and then dissolved in complete growth medium. The phenol-water or citric acid extracts of cementum shavings from periodontally diseased roots were positive for endotoxin by the limulus lysate assay (LLA). Pyrogen-free water extracts of diseased or phenol-water extracts of nondiseased cementum shavings were negative, or only slightly positive, respectively, for endotoxin by LLA. Media containing the various extracts were added to logarithmically growing cultures of human gingival fibroblasts (HGF). Separate cultures of HGF were exposed to Escherichia coli endotoxin at concentrations of 50, 100, 250 and 500 micrograms/ml to determine the growth-inhibitory effects of a known endotoxin. Cell growth was analyzed by measuring the incorporation of tritiated thymidine into cells. Suppression of HGF growth from 30 to 49% by E. coli endotoxin was concentration-dependent and linear over the concentration range of endotoxin tested. Pyrogen-free water extracts of diseased (endotoxin negative) or phenol-water extracts of nondiseased cementum shavings (slightly endotoxin positive) did not effect HGF growth. However, citric acid or phenol-water extracts of diseased cementum shavings (highly endotoxin positive) significantly suppressed HGF growth 58% and 61%, respectively. These results indicate that citric acid is effective in removing cytotoxic substances, presumably endotoxin, from cementum shavings and suggest that citric acid treatment is effective clinically in detoxifying periodontally diseased root surfaces.

Cell Division↗
PubMed1990

Crevicular fluid iron changes in treated and untreated periodontally diseased sites.

Previous investigations have shown that crevicular fluid iron concentration (CFIC) is higher in periodontally diseased sites. The present study was conducted to determine whether periodontal treatment changes the CFIC to levels found in healthy sites in the same persons. To test the significance of iron content in gingival fluid as an indicator of periodontal disease severity or activity, CFIC was determined for healthy sites and diseased sites treated with scaling and root planing alone or in conjunction with surgery both before and after treatment. CFIC was increased in diseased sites, but the iron concentration in crevicular fluid was not a good indicator of changes in disease severity resulting from periodontal treatment. Treatments produced an increase in the CFIC that may be more related to the status of the microcirculation than to the disease process itself.

Adult↗
PubMed1996

Clinical and pathomorphological investigation of spontaneously occurring periodontal disease in dogs.

Diagnostic evaluation of, and treatment planning for, different periodontal diseases of dogs are a common problem in veterinary dentistry. Therefore the aim of the present study was to propose a classification for inflammatory periodontal disease. One hundred and twenty-three male and female poodles (from two to over 12 years) were used for the clinical investigations; 120 periodontitis teeth were analysed for pathomorphological signs of inflammation. The recorded data made it possible to differentiate five forms of gingivitis (gingivitis simplex, hyperplastica, ulcerosa, granulomatosa and desquamativa) and three forms of periodontitis (juvenile, rapidly progressive adult and chronic adult periodontitis). The pathomorphological investigations allowed a differentiation between acute progressive inflammation, chronic nonprogressive inflammation, chronic proliferative inflammation and chronic resorptive inflammation. It is concluded that standardised diagnoses as well as the pathomorphological background may be helpful tools for providing effective treatment-strategies.

Animals↗
PubMed1982

Differing profiles of periodontal disease in two similar South Pacific island populations.

The periodontal condition of a cross-section of individuals aged between 15-59 years was characterised from clinical and radiographic observations of dental calculus, gingival inflammation, the level of the gingival attachment , alveolar bone loss, teeth missing or requiring extraction for periodontal reasons. The common characteristics of the profile in Tonga and W. Samoa were a high prevalence of the factors common to periodontal disease: calculus and gingival inflammation; a progressive apical movement of the gingival attachment; and alveolar bone loss. All these criteria showed a positive age dependency with calculus (particularly subgingival calculus) and gingival inflammation being very commonly associated with all tooth types at an early age, less than 30 years. Tooth loss observed was presumed to be previously associated with periodontal disease because the prevalence of dental caries was very low in both populations. Substantial differences were observed in the number of missing teeth between Tongan and Samoan populations, the Tongan subjects having a high rate of tooth loss. From radiographic interpretations of the periodontal conditions fewer subjects in Tonga were assessed as having no disease, and there was a higher prevalence of progressive destructive disease in Tonga than in W. Samoa. The proportion of subjects in both countries with no disease decreased rapidly with age. There was no evident explanation of the greater severity of disease in Tonga than in W. Samoa. The prevalence of microbial plaque, calculus and gingival inflammation was very high in all subjects at all ages particularly over 30 years in both populations.

Adolescent↗
PubMed2004

Diabetes, periodontal diseases, dental caries, and tooth loss: a review of the literature.

Diabetes mellitus, is a common chronic disease, and its prevalence in the United States, particularly type 2 diabetes, is increasing. Complications associated with diabetes impose a heavy burden on many people, especially among certain minority populations. Periodontal diseases, dental caries, and tooth loss also are common conditions in the United States, but their prevalence is generally decreasing. Nevertheless, among important subgroups of the population, particularly certain minority and economically disadvantaged groups, there is a disproportionately higher burden of periodontal diseases, dental caries, and tooth loss. This article reviews the post-1960 English-language literature on the relationship between diabetes and oral health, specifically focusing on periodontal disease, dental caries, and tooth loss. Substantial evidence exists to support the role of diabetes and poorer glycemic control as important risk factors for periodontal disease. Additionally, the evidence provides support for viewing the relationship between diabetes and periodontal diseases as bidirectional. However, additional research is necessary to firmly establish that treating periodontal infections can contribute to glycemic control management and possibly to the reduction of type 2 diabetes complications. The literature does not describe a consistent relationship between type 2 diabetes and dental caries. It reports increased, decreased, and similar caries experiences between those with and without diabetes. This review suggests that currently there is insufficient evidence to determine whether a relationship between diabetes and risk for coronal or root caries exists. Most of the reviewed studies reported greater tooth loss in people with diabetes. However, the differences were slight and not significant in several of the reports. Furthermore, this review of the association between diabetes and tooth loss reveals that valid population-based evidence generalizable to the US population is sparse. Further investigations of the association of diabetes with dental caries and tooth loss are warranted. If adverse effects of diabetes on dental caries and/or tooth loss are substantiated, the results of such studies would help design intervention studies to prevent or reduce the occurrence of dental caries and tooth loss in people with diabetes. These results also may affect existing clinical practice protocols and promote new public policy related to diabetes.

Blood Glucose↗
PubMed1989

Altered distribution of type I collagen mRNA in periodontal disease.

Earlier studies on collagen metabolism in the periodontium have suggested that periodontal disease is associated with reduced amounts of type I collagen in the pocket walls, and with an overall increase in collagen synthesis. In this study we analyzed gingival biopsies of patients suffering from adult type chronic periodontal disease by in situ hybridization, which permitted localization of fibroblasts containing different amounts of proa(I) collagen mRNA. The results showed that expression of type I collagen mRNA is reduced in the vicinity of periodontal pockets and dental plaque. Deeper in the connective tissue, high levels of proa(I) collagen mRNA were observed particularly around inflammatory cell infiltrates which may contribute to the fibrotic reaction observed. In all areas studied the levels of type I collagen mRNA in periodontal fibroblasts varied considerably, supporting previous views about their heterogeneity.

Collagen↗
PubMed2005

Periodontal diseases and the risk of preterm birth and low birth weight: a meta-analysis.

BACKGROUND: This meta-analysis of periodontal disease in relation to the risk of preterm birth/low birth weight (PTB/ LBW) is based on two case-control studies and three prospective cohort studies that met pre-stated inclusion criteria. METHODS: Information on the designs of the studies, characteristics of the study population, exposure and outcome measures, control for confounders, and risk estimates were abstracted independently by two investigators using a standard protocol. RESULTS: Pregnant women with periodontal disease had an overall adjusted risk of preterm birth that was 4.28 (95% confidence interval [CI], 2.62 to 6.99; P <0.005) times that risk for healthy subjects. The overall adjusted odds ratio of preterm low birth weight was 5.28 (95% CI, 2.21 to 12.62; P <0.005), while the overall adjusted odds ratio of a delivery of either PTB or LBW was 2.30 (95% CI, 1.21 to 4.38; P <0.005). CONCLUSIONS: Our findings indicate that periodontal diseases in the pregnant mother significantly increase the risk of subsequent preterm birth or low birth weight. While it remains important to promote good oral hygiene during routine prenatal visits, there is no convincing evidence, on the basis of existing case control and prospective studies, that treatment of periodontal disease will reduce the risk of preterm birth. Consequently, large randomized, placebo-controlled, masked clinical trials are required.

Female↗
PubMed2002

Alterations of neutrophil f-actin kinetics by tobacco smoke: implications for periodontal diseases.

Tobacco smoking is a major risk factor in the incidence and severity of periodontal diseases. Alterations of neutrophil function by short-term high levels of smoke during the act of smoking (acute smoke exposure) as well as long-term exposure to lower levels of tobacco substances in the bloodstream (chronic smoke exposure) may play a role in the pathogenesis of periodontal diseases in smokers. The polymerization and depolymerization of f-actin in response to infectious agents or inflammatory mediators is a critical process in a variety of neutrophil functions. In this study, we examined the effects of in vitro smoke exposure on neutrophils from smokers and non-smokers (which may be comparable to in vivo acute smoke exposure) and neutrophils from smokers not exposed to further in vitro smoke (which may be comparable to chronic smoke exposure) on f-actin kinetics. Peripheral neutrophils were isolated from seven healthy smoking subjects and seven healthy age-matched non-smoking subjects and exposed to 1-5 min of acute smoke in a smoke box system or not exposed to further smoke (baseline controls). Selected aliquots of neutrophils from control and 5-min exposures of acute smoke were then stimulated with the chemotactic peptide F-met-leu-phe at 10(-7) M for an additional 30-360 s. Cells were fixed and permeabilized, stained for f-actin with NBD phallacidin, and analyzed by flow cytometry. From baseline to 5 min of in vitro smoke exposure, there was a 38% decline in f-actin stain in non-smokers and a 30% decline in f-actin stain in smokers (p > 0.05) with f-actin values slightly higher in smokers than-non-smokers (p > 0.05). With F-met-leu-phe stimulation, both smokers and-non-smokers demonstrated a characteristic rise in f-actin stain from 0 to 120 s with a subsequent decline to baseline at 360 s and no significant differences in f-actin levels at any time of stimulation between groups. After preincubation with 5 min of in vitro smoke, the magnitude of rise in f-actin was less in both smokers and non-smokers when compared to cells not incubated with 5 min of smoke (p < 0.05 at 120 s for both smokers and non-smokers). F-actin values in smokers were higher than-non-smokers from 30 to 360 s of F-met-leu-phe exposure (p > 0.05). These results demonstrate that in vitro smoke exposure may impair normal f-actin kinetics. These alterations in f-actin kinetics may in turn affect other neutrophil functions which may impact on the pathogenesis of periodontal diseases in smokers.

Actins↗