The effect of alcohol consumption on periodontal disease.

BACKGROUND: Alcohol consumption, like smoking, may be related to periodontal disease independently of oral hygiene status. This study assessed the relationship between alcohol consumption and severity of periodontal disease. METHODS: A cross-sectional study of 1,371 subjects ages 25 to 74 in the Erie County, NY population was performed. Alcohol intake was assessed by means of previously validated self-reported questionnaires. Outcome variables were gingival bleeding, clinical attachment loss, alveolar bone loss, and presence of subgingival microorganisms. RESULTS: Logistic regression analyses adjusting for age, gender, race, education, income, smoking, diabetes mellitus, dental plaque, and presence of any of 8 subgingival microorganisms showed that those consuming > or =5 drinks/week had an odds ratio (OR) of 1.65 (95% CI: 1.22 to 2.23) of having higher gingival bleeding, and OR of 1.36 (95% CI: 1.02 to 1.80) of having more severe clinical attachment loss compared to those consuming <5 drinks/week. Those consuming > or =10 drinks/week had an odds ratio (OR) of 1.62 (95% CI: 1.12 to 2.33) of having higher gingival bleeding and OR of 1.44 (95% CI: 1.04 to 2.00) of having more severe clinical attachment loss compared to those consuming <10 drinks/week. Alcohol consumption was not significantly related to alveolar bone loss nor to any of the subgingival microorganisms. CONCLUSIONS: The results suggest that alcohol consumption is associated with moderately increased severity of periodontal disease. Longitudinal studies are needed to determine whether alcohol is a true risk factor for periodontal disease.

Treatment of periodontal disease and control of diabetes: an assessment of the evidence and need for future research.

Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha. Genetics, age, and, nutrition are important signals for this increased response and as reported more recently, infections and inflammation. Persistent elevation of IL-1 beta, IL-6, and TNF-alpha in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. In addition, TNF-alpha, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. Collectively, the evidence supports a role for cytokine elevation in the pathophysiology and metabolic abnormalities associated with diabetes. Periodontitis is an infection that is twice as prevalent in diabetic individuals compared to non-diabetics. Porphyromonas gingivalis, one of the microorganisms responsible for this infection, is able to invade endothelial cells and is a potent signal for monocyte and macrophage activation. Thus, once established in the diabetic host, this chronic infection complicates diabetes control and increases the occurrence and severity of microvascular and macrovascular complications. Unlike treatment of acute infections, modalities of treatment for chronic infections are a matter of debate. Evidence indicates that mechanical removal of subgingival infection does not result in complete elimination of periodontal infection and consequently there is no effect on diabetes control measured as reduction in glycated hemoglobin. On the other hand, studies incorporating systemic antibiotics as adjuncts to mechanical debridement result in a reduction of P. gingivalis to nondetectable levels and a concomitant reduction in glycated hemoglobin, independent of the hypoglycemic effects of diabetes drugs or insulin. The evidence supports the notion that treatment of chronic periodontal infection is essential in the diabetic patient. Assessment of infection status in diabetic patients is fundamental for appropriate treatment decisions.

The relationship between bone mineral density and periodontitis in postmenopausal women.

BACKGROUND: Systemic bone loss has been proposed as a risk factor for periodontal disease; however, the relationship between these two diseases is still not clear. The objective of this study was to assess the relationship between systemic bone mineral density and periodontal disease, controlling for known confounders. METHODS: The study population included 70 postmenopausal Caucasian women aged 51 to 78 (mean +/- SD: 62.10 +/- 7.1 years). Skeletal bone mineral density (BMD) was assessed by dual energy x-ray absorptiometry (DXA) at the neck, trochanter, intertrochanter, Ward's triangle, and total regions of the femur, and from the anterior-posterior view of the lumbar spine. Periodontal disease severity was represented by clinical attachment loss (CAL) and interproximal alveolar bone loss (ABL). Other measures of periodontal status included probing depth (PD), supragingival plaque, gingival bleeding on probing, and calculus. DXA and oral examinations were performed by calibrated examiners. Partial correlation coefficients (r) were obtained from multiple linear regression analysis adjusting for age, age at menopause, estrogen supplementation, cigarette smoking, body mass index, and supragingival plaque. RESULTS: Mean ABL was significantly correlated with BMD of the trochanter (r =- 0.27), Ward's triangle (r = -0.26), and total regions of the femur (r = -0.25). Mean CAL appeared to be related to BMD consistently at all regions of the skeleton, although the association did not reach statistical significance. CONCLUSIONS: We can conclude that skeletal BMD is related to interproximal alveolar bone loss and, to a lesser extent, to clinical attachment loss, implicating postmenopausal osteopenia as a risk indicator for periodontal disease in postmenopausal Caucasian women.

Dietary vitamin C and the risk for periodontal disease.

BACKGROUND: Vitamin C has long been a candidate for modulating periodontal disease. Studies of scorbutic gingivitis and the effects of vitamin C on extracellular matrix and immunologic and inflammatory responses provide a rationale for hypothesizing that vitamin C is a risk factor for periodontal disease. METHODS: We evaluated the role of dietary vitamin C as a contributing risk factor for periodontal disease utilizing the Third National Health and Nutrition Examination Survey (NHANES III) which is representative of the U.S. civilian, non-institutionalized population. RESULTS: A sample of 12,419 adults (20 to 90+ years of age), with dental measurements and assessment of dietary information as well as demographic and medical histories were included in the studies. Dietary vitamin C was estimated by a 24-hour dietary record. Individuals with periodontal disease were arbitrarily defined as those who had mean clinical attachment levels of > or =1.5 mm. Using multiple logistic regression analysis, we found a relationship between reduced dietary vitamin C and increased risk for periodontal disease for the overall population (odds ratio [OR] = 1.19; 95% CI: 1.05 to 1.33). Current and former tobacco users who were taking less dietary vitamin C showed an increased risk of periodontal disease with OR of 1.28, 95% CI: 1.04 to 1.59 for former smokers, and an OR of 1.21, 95% CI: 1.02 to 1.43 for current tobacco users. There was a dose-response relationship between the levels of dietary vitamin C and periodontal disease with an OR of 1.30 for those taking 0 to 29 mg of vitamin C per day, to 1.16 for those taking 100 to 179 mg of vitamin C per day as compared to those taking 180 mg or more of vitamin C per day. CONCLUSION: Dietary intake of vitamin C showed a weak, but statistically significant, relationship to periodontal disease in current and former smokers as measured by clinical attachment. Those taking the lowest levels of vitamin C, and who also smoke, are likely to show the greatest clinical effect on the periodontal tissues.

Calcium and the risk for periodontal disease.

BACKGROUND: Dietary calcium has long been a candidate to modulate periodontal disease. Animal as well as human studies of calcium intake, bone mineral density, and tooth loss provide a rationale for hypothesizing that low dietary intake of calcium is a risk factor for periodontal disease. METHODS: We evaluated the role of dietary calcium intake as a contributing risk factor for periodontal disease utilizing the Third National Health and Nutrition Examination Survey (NHANES III), which is representative of the U.S. civilian non-institutionalized population. Dietary calcium intake was determined from a 24-hour dietary recall. The U.S. Department of Agriculture Nutrient Database was used as a source of nutrient composition data. Periodontal disease was measured by attachment loss. In addition, serum calcium was assessed using venous blood samples. Logistic regression analysis was used to examine the association between periodontal disease and dietary calcium intake or serum calcium levels after adjusting for covariants including age, gender, tobacco consumption, and gingival bleeding. RESULTS: The association of lower dietary calcium intake with periodontal disease was found for young males and females (20 to 39 years of age), and for older males (40 to 59 years of age). The relationship between low dietary calcium intake and increased levels of periodontal disease showed an estimated odds ratio (OR) of 1.84 (95% CI: 1.36 to 2.48) for young males, 1.99 (95% CI: 1.34 to 2.97) for young females, and 1.90 (95% CI: 1.41 to 2.55) for the older group of males. These odds ratios were adjusted for gingival bleeding and tobacco consumption. The dose response was also seen in females, where there was 54% greater risk of periodontal disease for the lowest level of dietary calcium intake (2 to 499 mg) and 27% greater risk in females who took moderate levels of dietary calcium (500 to 799 mg) as compared to those who took 800 mg or more dietary calcium per day. A statistically significant association between low total serum calcium and periodontal disease was found in younger females aged 20 to 39 with OR = 6.11 (95% CI: 2.36 to 15.84) but not for males or older females, after adjusting for tobacco use, gingival bleeding, and dietary calcium intake. CONCLUSIONS: These results suggest that low dietary intake of calcium results in more severe periodontal disease. Further studies will be needed to better define the role of calcium in periodontal disease and to determine the extent to which calcium supplementation will modulate periodontal disease and tooth loss.

Relationship of stress, distress and inadequate coping behaviors to periodontal disease.

BACKGROUND: The association of stress, distress, and coping behaviors with periodontal disease was assessed. METHODS: A cross-sectional study of 1,426 subjects between the ages of 25 and 74 years in Erie County, New York, was carried out to assess these relationships. Subjects were asked to complete a set of 5 psychosocial questionnaires which measure psychological traits and attitudes including discrete life events and their impact; chronic stress or daily strains; distress; coping styles and strategies; and hassles and uplifts. Clinical assessment of supragingival plaque, gingival bleeding, subgingival calculus, probing depth, clinical attachment level (CAL) and radiographic alveolar crestal height (ACH) was performed, and 8 putative bacterial pathogens from the subgingival flora measured. RESULTS: Reliability of subjects' responses and internal consistencies of all the subscales on the instruments used were high, with Cronbach's alpha ranging from 0.88 for financial strain to 0.99 for job strain, uplifts, and hassles. Logistic regression analysis indicated that, of all the daily strains investigated, only financial strain was significantly associated with greater attachment and alveolar bone loss (odds ratio, OR = 1.70, 95% CI = 1.09 to 2.65 and OR = 1.68, 95% CI = 1.20 to 2.37, respectively) after adjusting for age, gender, and cigarette smoking. When coping behaviors were evaluated, it was found that those with more financial strain who were high emotion-focused copers (a form of inadequate coping) had a higher risk of having more severe attachment loss (OR = 2.24, 95% CI = 1.15 to 4.38) and alveolar bone loss (OR = 1.91, 95% CI = 1.15 to 3.17) than those with low levels of financial strain within the same coping group, after adjustment for age, gender, and cigarette smoking. Similar results were found among the low problem-focused copers for AL (OR = 2.21, 95% CI = 1.11 to 4.38) and ACH (OR = 2.12, 95% CI = 1.28 to 3.51). However, subjects with high levels of financial strain who reported high levels of problem-based coping (considered adequate or good coping) had no more periodontal disease than those with low levels of financial strain, suggesting that the effects of stress on periodontal disease can be moderated by adequate coping behaviors. CONCLUSIONS: We find that psychosocial measures of stress associated with financial strain and distress manifest as depression, are significant risk indicators for more severe periodontal disease in adults in an age-adjusted model in which gender (male), smoking, diabetes mellitus, B. forsythus, and P. gingivalis are also significant risk indicators. Of considerable interest is the fact that adequate coping behaviors as evidenced by high levels of problem-based coping, may reduce the stress-associated risk. Further studies also are needed to help establish the time course of stress, distress, and inadequate coping with respect to the onset and progression of periodontal disease, and the mechanisms that explain this association.

Periodontal disease and diabetes mellitus: a two-way relationship.

Severe periodontal disease often coexists with severe diabetes mellitus. Diabetes is a risk factor for severe periodontal disease. A model is presented whereby severe periodontal disease increases the severity of diabetes mellitus and complicates metabolic control. We propose that an infection-mediated upregulation cycle of cytokine synthesis and secretion by chronic stimulus from lipopolysaccharide (LPS) and products of periodontopathic organisms may amplify the magnitude of the advanced glycation end product (AGE)-mediated cytokine response operative in diabetes mellitus. In this model, the combination of these 2 pathways, infection and AGE-mediated cytokine upregulation, helps explain the increase in tissue destruction seen in diabetic periodontitis, and how periodontal infection may complicate the severity of diabetes and the degree of metabolic control, resulting in a 2-way relationship between diabetes mellitus and periodontal disease/infection. This proposed dual pathway of tissue destruction suggests that control of chronic periodontal infection is essential for achieving long-term control of diabetes mellitus. Evidence is presented to support the hypothesis that elimination of periodontal infection by using systemic antibiotics improves metabolic control of diabetes, defined by reduction in glycated hemoglobin or reduction in insulin requirements.

Models to evaluate the role of stress in periodontal disease.

We evaluated the association of stress,distress, and coping behaviors with periodontal disease in 1,426 subjects, aged 25 to 74, in Erie County, NY, Demographic characteristics, medical and dental history, and tobacco and alcohol consumption, as well as clinical assessments of supragingival plaque, subgingival flora, gingival bleeding, calculus, probing depth, clinical attachment level (CAL), and radiographic alveolar bone loss (ABL) were obtained for each subject. Subjects also completed a set of 5 psychosocial instruments that measured life events, daily strains, hassles and uplifts, distress, and coping behaviors. Internal consistencies of all subscales on the instruments were high, with Cronbach's alpha ranging from 0.88 to 0.99. Logistic regression indicated that financial strain was significantly associated with greater attachment and alveolar bone loss (OR 1.70; 95% CI, 1.09-2.65; and 1.68; 95% CI, 1.20-2.37, respectively) after adjusting for age, gender, and smoking. When those with financial strain were stratified with respect to coping behaviors, it was found that those who exhibited high emotion-focused coping (inadequate coping) had and even higher risk of having more severe attachment loss (OR 2.24; 95% CI, 1.15-4.38) and alveolar bone loss (OR 1.91; 95% CI, 1.15-3.17) than those with low levels of financial strain within the same coping group, after adjustment for age, gender, and cigarette smoking. After further adjusting for number of visits to the dentist, those with financial strain who were high emotion-focused copers still had higher levels of periodontal disease based on CAL (OR 2.12; 95% CI, 1.07-4.18). In contrast, subjects with high levels of financial strain who reported high levels of problem-based coping (good coping) had no more periodontal disease than those with low levels of financial strain. Salivary cortisol levels were higher in a test group exhibiting severe periodontitis, a high level of financial strain, and high emotion-focused coping, as compared to a control group consisting of those with little or no periodontal disease, low financial strain, and low levels of emotion-focused coping (11.04 +/-4.4 vs/ 8.6 +/- 4.1 nmol/L salivary cortisol, respectively). These findings suggest that psychosocial measures of stress associated with financial strain are significant risk indicators for periodontal disease in adults. Further prospective studies are needed to help establish the time course of stress, distress, and inadequate coping on the onset and progression of periodontal disease, as well as to evaluate the mechanisms by which stress exerts its effects on periodontal infections.

Radiographic and clinical responses to periodontal therapy.

Mechanical periodontal therapy is widely used for a variety of periodontal conditions. While the clinical efficacy of this treatment has been validated, the radiographic response has not been studied in depth. The purpose of the present study was to examine the clinical and radiographic response to mechanical periodontal therapy, and assess the factors associated with these changes. One hundred and eight patients, with established periodontitis, received oral hygiene instruction and mechanical periodontal therapy for a period of 4 to 5 weeks. Scheduled maintenance visits were performed at 3, 6, 9, and 15 months. Probing depth (PD) and attachment level (AL) measurements were performed at baseline, and at 3 and 15 months. Intraoral radiographs were taken at baseline and 12 to 15 months postsurgery using a Rinn alignment system. Alveolar crestal height (ACH) measurements were performed on a pair of digitized images of the previously taken radiographs. An overall mean of patients' changes for PD, AL, and ACH was initially computed. Active sites (gainers and losers) were determined using a threshold method, and expressed as patient's percentage of active sites (number of active sites of the total sites measured in each patient). Mean overall probing reduction and AL gain was 0.5 mm and 0.44 mm, respectively. Of all sites measured, 16.6% exhibited AL gain, while only 6.2% of all sites exhibited AL loss. Mean overall change in ACH was -0.07 mm, of which 11.8% of all sites exhibited ACH gain, while 15.1% exhibited loss beyond the threshold. Non-smokers presented no change in bone loss, while smokers continued to lose bone at an annual rate of 0.17 mm, despite treatment (P <0.005). Likewise, the average percent of sites per patients showing attachment gain beyond the threshold were much greater in non-smokers (13.9%) compared to 9.0% in smokers (P <0.01). Mean probing reduction was 50% greater among non-smokers (0.6 mm) when compared to smokers (0.4 mm), which was also statistically significant (P <0.05). A positive and significant correlation was established between the percentage of sites with AL gain and sites with ACH gain (Rho =0.40; P=0.0001). It is suggested that monitoring sites for AL and ACH gain expressed as changes beyond a selective threshold is an important outcome variable in treatment studies.

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.

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.

Reliability of a self-reported health questionnaire in a periodontal disease study.

This study assesses the reliability of a self-reported health questionnaire completed by 413 subjects aged 25-74 yr in the Erie County Periodontal Disease (ECPD) Study. Specific questions on general and oral health conditions were completed by each subject during a first visit and at a follow-up examination 2 yr later, and the two compared. Results showed that the overall measure of agreement between the two visits is substantial (average kappa, kappa = 0.80). Variation by gender and age were minimal. Questions regarding allergy to medications, oral treatment, reason for tooth extraction, health symptoms and history of systemic diseases exhibited high levels of agreement (kappa ranged from 0.71-0.90). Information on vitamin and mineral intake yielded kappa = 0.63. Oral conditions scored the lowest but were still acceptable (kappa = 0.57). These findings indicate that there were no significant discrepancies in self-reported responses to the health questionnaire used in the ECPD Study. Although the information provided by the subject may not be as accurate as compared to laboratory testing, it is nevertheless a reliable source of information which can be utilized cost-effectively in research studies.

The relationship between radiographic and clinical changes in the periodontium.

Change in clinical attachment level (CAL) and radiographic change in crestal bone height are often used to assess periodontal breakdown and disease progression. These two variables are also used to monitor the effect of treatment. The purpose of the present longitudinal study was to evaluate the correlation between changes in CAL and alveolar bone loss. Following initial screening, 79 subjects with established periodontitis were monitored quarterly for 1 yr, using a pressure-sensitive automated probe. CAL and relative attachment level (RAL) were recorded at 6 sites for each tooth. Radiographs were obtained at baseline and 1 yr. Crestal bone changes were determined using an image enhancement technique. Mean change in attachment level was 0.16 mm. Similarly, mean proximal bone loss measured radiographically was 0.16 mm. In 6.9% of all the sites, and 13.7% of all pooled interproximal sites, AL loss was in excess of the threshold defined as 2 s.d. of repeated measurements (mean 1.54 mm). Similar percentages of sites (12.9%) had radiographic evidence of proximal bone loss exceeding the threshold (0.55-1.08 mm). A site-based analysis of active sites revealed an overall poor correlation between the 2 variables (kappa value = 0.03) which was the result of a very poor sensitivity (0.16) despite a relatively good specificity (0.81). A patient-based comparison of clinical and radiographical changes revealed an overall kappa value of 0.08, with sensitivity and specificity of 0.51 and 0.56, respectively. However, baseline CAL and crestal bone height showed good correlation (r = 0.73; p = 0.0001). It is suggested that changes in CAL and radiographic bone level progress somewhat independently. Over a short-term period of time they might not follow the same course; however, in the long term, these differences seem to level off. For longitudinal monitoring of disease progression and response to therapy both methods may be needed; while for cross-sectional evaluation and long-term prospective studies, either variable may be used alone.

Treatment of periodontal disease in diabetics reduces glycated hemoglobin.

Periodontal disease is a common infection-induced inflammatory disease among individuals suffering from diabetes mellitus. The purpose of this study was to assess the effects of treatment of periodontal disease on the level of metabolic control of diabetes. A total of 113 Native Americans (81 females and 32 males) suffering from periodontal disease and non-insulin dependent diabetes mellitus (NIDDM) were randomized into 5 treatment groups. Periodontal treatment included ultrasonic scaling and curettage combined with one of the following antimicrobial regimens: 1) topical water and systemic doxycycline, 100 mg for 2 weeks; 2) topical 0.12% chlorhexidine (CHX) and systemic doxycycline, 100 mg for 2 weeks; 3) topical povidone-iodine and systemic doxycycline, 100 mg for 2 weeks; 4) topical 0.12% CHX and placebo; and 5) topical water and placebo (control group). Assessments were performed prior to and at 3 and 6 months after treatment and included probing depth (PD), clinical attachment level (CAL), detection of Porphyromonas gingivalis in subgingival plaque and determination of serum glucose and glycated hemoglobin (HbA1c). After treatment all study groups showed clinical and microbial improvement. The doxycycline-treated groups showed the greatest reduction in probing depth and subgingival Porphyromonas gingivalis compared to the control group. In addition, all 3 groups receiving systemic doxycycline showed, at 3 months, significant reductions (P < or = 0.04) in mean HbA1c reaching nearly 10% from the pretreatment value. Effective treatment of periodontal infection and reduction of periodontal inflammation is associated with a reduction in level of glycated hemoglobin. Control of periodontal infections should thus be an important part of the overall management of diabetes mellitus patients.

Effect of mechanical treatment on healing after third molar extraction.

The aim of this study was to determine the effect of subgingival scaling and root planing on healing of the distal surface of second molars following extraction of third molars. Twenty-eight patients with contralateral erupted third molars and pocket depths greater than or equal to 3 mm on the distal surface of the second molars participated in this study. Measurements of supragingival bacterial plaque, bleeding on probing, pocket depth, and relative attachment level were performed at baseline and 2 months after treatment. Extraction of contralateral third molars was carried out simultaneously. The experimental site received thorough scaling and root planing of the distal surface of the second molar, while the control site received extraction alone. Experimental sites showed significant improvement in all clinical parameters assessed compared to the control sites. In conclusion, periodontal lesions on the distal of second molars can be significantly improved following scaling and root planing after extraction of third molars.

Effects of smoking and smoking cessation on healing after mechanical periodontal therapy.

This study investigated the effect of cigarette smoking on 143 patients' clinical and microbiological responses to mechanical therapy. Treatment included four to six sessions of subgingival scaling and root planing and instruction in oral hygiene. Results indicate that current smokers have less healing and reduction in subgingival Bacteroides forsythus and Porphyromonas gingivalis after treatment compared to former and nonsmokers, suggesting that smoking impairs periodontal healing. As the healing and microbial response of former smokers is comparable to that of nonsmokers, smoking cessation may restore the normal periodontal healing response.

Longitudinal study of prognostic factors in established periodontitis patients.

Numerous indicators for disease progression have been described in the last decade. The purpose of this study was to examine, longitudinally, a large battery of clinical, microbiological, and immunological indicators, to try to determine whether the presence of one or a combination of these parameters at baseline, would correlate positively with increased attachment and or bone loss (true prognostic factors). Following initial screening, 79 patients with established periodontitis were monitored longitudinally for one year. Whole mouth clinical measurements, plaque gingival and calculus indices, together with pocket depth and attachment level measurements, were repeated every three months. Full mouth radiographic survey, performed at baseline and 12 months, served to determine changes in crestal bone height using an image enhancement technique. Subgingival plaque samples were taken at baseline and every 3 months. Immunofluorescence assays were performed for the a battery of target microorganisms. Serum and GCF samples for IgG subclasses analysis were obtained at each visit and assayed using ELISA techniques. Likewise blood, samples were also drawn at each visit for a quantitative analysis of serum cotinine level. The overall mean attachment loss (AL) and bone loss (BL) were almost identical (0.159 mm and 0.164 mm, respectively). Individual patients variation was large (-0.733 to +1.004 mm). An overall 6.89% of sites were active; individual patients' means ranged from 0-28.9%. Mean pocket depth (PD) showed minimal change over the study period (-0.033 mm) thus suggesting that most if not all the AL was accompained by concomitant gingival recession. Smokers exhibited greater AL and radiographic BL compared to non-smokers. Likewise, patients' cotinine level showed direct correlation with outcomes of progressive periodontal breakdown. Past severity of periodontal involvement, as reflected in the patients baseline PD, AL and crestal bone height, showed good correlation with longitudinal changes in the periodontium. This correlation was higher for crestal BL as the outcome variable, while somewhat smaller for change in AL as the outcome variable. Bacteroides forsythus (Bf.), Prevotella intermedia (Pi.) and Porphyromonas gingivalis (Pg.) were frequently found in these patients. The presence of these microorganisms at baseline was associated with further disease progression. Subjects with mean baseline pocket depth equal or greater than 3.2 mm were at greater risk for future bone loss 1 year later (O.R. 2.97; C.I. 1.02-8.70). Smokers were at significantly greater risk for further attachment loss when compared to non-smokers (O.R. 5.41; C.I. 1.50-19.5). Subjects that harbored B. forsythus at baseline, were at seven times greater risk for increased pocket depth (O.R. 7.84; C.I.1.74-35.3). In conclusion, past periodontal destruction, smoking habits, Bf., Pg., & Pi. are prognostic factors for further periodontal breakdown. When designing clinical trials, or when evaluating epidemiological data, it is most important to balance for these factors. Also, treatment strategies should attempt to eliminate or modify these factors.

Cigarette smoking increases the risk for subgingival infection with periodontal pathogens.

Cigarette smoking has been found to increase the risk for periodontitis. The present study examined the association between cigarette smoking and subgingival infection with periodontal pathogens to determine if smokers are more likely to be infected with certain periodontal pathogens than non-smokers. Self-reported data on 1,426 subjects, aged 25 to 74, from the Erie County Study were obtained including data on 798 subjects who were current or former smokers. Mean clinical attachment loss was used to estimate the severity of periodontal destruction. Subgingival infection with target periodontal pathogens was determined by indirect immunofluorescence microscopy. Smokers harbored significantly higher levels and were at significantly greater risk of infection with Bacteroides forsythus than non-smokers. Adjusting for disease severity, the risk of subgingival infection with B. forsythus in current smokers was 2.3 times that of former smokers or non-smokers. The relative risk of B. forsythus infection also increased 1.18 times for every category of smoking as the amount of smoking measured in packyears increased from very light to heavy. Adjusting for disease severity, Porphyromonas gingivalis was also more likely to subgingivally infect smokers than non-smokers; however, there was not a significantly higher relative risk for infection with this bacterium. The data from this study indicate that cigarette smoking increases the likelihood of subgingival infection with certain periodontal pathogens. This may partly explain the increased risk for periodontitis seen in smokers.

The role of osteopenia in oral bone loss and periodontal disease.

Osteoporosis and periodontitis are diseases which affect a large number of women and men, with incidence increasing with advancing age. Osteopenia is a reduction in bone mass due to an imbalance between bone resorption and formation, favoring resorption, resulting in demineralization and leading to osteoporosis. Osteoporosis is a disease characterized by low bone mass and fragility and a consequent increase in fracture risk. Periodontitis is characterized by inflammation of the supporting tissues of the teeth, resulting in resorption of the alveolar bone as well as loss of the soft tissue attachment to the tooth and is a major cause of tooth loss and edentulousness in adults. The relationship of osteopenia to oral bone loss and periodontal disease has been addressed in a limited number of studies. A review of current knowledge regarding this relationship is presented. Interpretation of the literature is complicated by the variety of methods used to assess osteopenia, oral bone mass, and periodontitis, as well as varying definitions of outcomes of interest. Results of a previously unpublished study are presented which suggest that severity of osteopenia is related to loss of alveolar crestal height and tooth loss in post-menopausal women. The literature on the relationship among these disorders is limited and points to the need for additional studies which thoroughly evaluate the influence of potential confounding factors to further define the relationship between low bone mineral density and periodontal disease in larger populations. Clearer understanding of this relationship may aid health care providers in their efforts to detect and prevent osteoporosis and periodontal disease. Increased dialogue among medical and dental professional will be increasingly important in achieving and maintaining patients' optimal health.

Response to periodontal therapy in diabetics and smokers.

Diabetics and smokers are two patient groups at high risk for periodontal disease who also exhibit impaired wound healing and, therefore, constitute two different groups in whom the relationship between host-parasite interaction, outcome of periodontal therapy, and systemic factors is best represented. The results of two independent clinical trials involving treatment of periodontal disease in diabetics and smokers are presented. A new treatment regimen for the management of periodontal disease associated with diabetes mellitus is proposed. This treatment approach incorporates both antimicrobial agents and pharmacological modulation of the host response. Elimination of periodontal infection and reduction of periodontal inflammation in diabetic patients resulted in a significant short-term reduction in the concentration of glycosylated hemoglobin (HbA1c). Control of chronic infections and modulation of the host response offer a new therapeutic approach in the management of patients with both diabetes and periodontal disease. The effect of smoking on periodontal healing is also discussed. The clinical and microbiological response of smokers to non-surgical periodontal therapy is compared to non-smokers. In addition, possible mechanisms whereby diabetes mellitus and cigarette smoking increase the severity of periodontal disease are discussed.