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Periodontal disease: an overview for physicians.

Periodontitis is now seen as resulting from a complex interplay of bacterial infection and host response, often modified by behavioral factors. There has been a fundamental change in the prevailing periodontal disease model of the 1960s, which suggested that the susceptibility to periodontitis increases with age, and that all individuals are susceptible to severe periodontal disease. More recent research has changed the belief in universal susceptibility to the current view that only some 5-20% of any population suffer from severe generalized periodontitis, and that only moderate disease affects a majority of adults. One major risk factor is smoking, as there is now a clear association between smoking and periodontal disease independent of oral hygiene, age, or any other risk factor. In human periodontitis, there is no simple, direct pathogen-disease link. There are three pathogens that have a strong association with progressive periodontal disease: Actinobacillus actinomycetemcomitans, spirochetes of acute necrotizing gingivitis, and Porphyromonas gingivalis. These pathogens may be the cause of continued loss of periodontal attachment in all periodontal disease classifications despite diligent periodontal therapy. This loss of attachment, or destruction of the periodontal ligament and loss of adjacent supporting bone, is seen in adult periodontitis, as well as in early-onset periodontitis, which affects young persons who otherwise appear healthy. The three forms of early-onset periodontitis are prepubertal periodontitis, localized and generalized juvenile periodontitis, and rapidly progressive periodontitis. They are distinguished from adult periodontitis by the age of onset of the disease, the rapid rate of disease progression, manifestations of defects in host response, and the composition of the subgingival microflora. Prepubertal periodontitis is associated with attachment loss around teeth of the deciduous and/or permanent dentition, and is often associated with severe congenital defects of hematological origin, and alterations in neutrophil chemotaxis function. Periodontitis may also be associated with systemic conditions such as metabolic disorders (diabetes mellitus, female hormonal alterations), drug-induced disorders, hematologic disorders/leukemia, and immune system disorders. These systemic disorders have been documented as capable of affecting the periodontium and/or treatment of periodontal disease. In order to rationally treat and prevent periodontal disease, we need to know the etiologic agents for specific patients, and the mechanism of bacterial pathogenesis in periodontitis. In systemic diseases in which the periodontal tissues are affected as well, early detection and carefully managed therapeutics with the physician and periodontist working together may prove beneficial to the patient's general health and quality of life.

Adult↗

PubMed1998

Genetic variations in cytokine expression: a risk factor for severity of adult periodontitis.

Periodontitis is a collection of chronic inflammatory diseases that are caused by specific bacteria. The bacteria activate inflammatory mechanisms in the periodontal tissues that destroy collagen and bone that support the teeth. Although bacteria are essential for the initiation of periodontitis, the quantity and types of bacteria have not been sufficient to explain the differences in disease severity. In recent years, it has become evident that for many common chronic diseases, there are modifying factors that do not cause the disease but rather amplify some disease mechanisms to make the clinical condition more severe. There are now data to suggest that a few factors which amplify the inflammatory process make people susceptible to an increased severity of periodontitis. Studies of untreated disease in Sri Lanka identified 3 patterns of disease progression. Studies in twins suggested that part of the clinical characteristics of periodontitis may be explained by genetic factors, but previous attempts to identify genetic markers for periodontitis have been unsuccessful Some genetic variations (polymorphisms) are commonly found in our population and represent a mechanism by which individuals may exhibit variations within the range of what is considered biologically normal. Since certain cytokines are key regulators of the inflammatory response and are important in periodontitis, we investigated the relationship between genetic variations associated with cytokine production and periodontitis severity. There are several polymorphisms in the cluster of genes that influence IL-1 biological activity. In recent clinical trials, two of these polymorphisms, when found together, have been associated with a significant increase in the risk for severe generalized periodontitis. Genetic association with periodontitis was evident only when smokers were excluded from the analysis, confirming the importance of smoking, and suggesting that both smoking and the IL- I genotype are independent factors in severe periodontitis. It is notable that 1 polymorphism associated with severe periodontitis in our study is also known to correlate with a 2- to 4-fold increase in IL-1 beta production. These findings are consistent with the current model of how genetic factors influence common chronic diseases. If we apply this model to periodontitis, it would involve the following: 1) a disease-initiating factor that would undoubtedly be specific bacteria such as Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans. and Bacteroides forsythus: and 2) modifiers of disease mechanisms that account for the clinical severity, including smoking, the IL-I genotype, certain systemic diseases, and psychosocial stress. The association of the IL-I genotype with severe periodontitis is consistent with several lines of periodontal research. Several studies have suggested there is a substantial genetic influence in periodontal disease. Although specific genetic markers have been identified in the uncommon juvenile forms of periodontitis, previous studies of specific genetic markers in adults with periodontitis have not been encouraging. Many investigators have, however, demonstrated a role for IL-1 in the initiation and progression of periodontitis. For example, IL-1 activates the degradation of the extracellular matrix and bone of the periodontal tissues, and elevated tissue or gingival fluid levels of IL-1 beta have been repeatedly associated with periodontitis. In addition, IL-1 is a strong enhancer of tissue levels of PGE2 and TNF-alpha. The association of severe periodontitis with smoking and the IL-1 genotype suggest a role for these factors in the pathogenesis of periodontitis. The finding that host modifying factors are associated with severe periodontitis suggest a biological mechanism by which some individuals, if challenged by bacterial accumulations, may have a more vigorous immunoinflammatory response, leading to more severe clinical disease. (ABSTRACT

Adult↗

PubMed2005

Relationship of Actinobacillus actinomycetemcomitans serotypes to periodontal condition: prevalence and proportions in subgingival plaque.

No study available has utilized the new classification scheme (the consensus report of the American Academy of Periodontology 1999) to determine the prevalence of Actinobacillus actinomycetemcomitans in different periodontal conditions. The purpose of this study was to investigate prevalence and proportions of A. actinomycetemcomitans serotypes in subgingival plaque samples from a young Taiwanese population with aggressive periodontitis, chronic periodontitis and no periodontal disease. A total of 221 subgingival plaque samples from 171 diseased subjects (70 had aggressive periodontitis, and 101 had chronic periodontitis) (mean age 25.0 +/- 8.2 yr) and 50 periodontally healthy subjects (mean age 18.4 +/- 9.5 yr) were screened for A. actinomycetemcomitans. Serotypes of A. actinomycetemcomitans were determined by an indirect immunofluorescence assay using serotype-specific polyclonal antisera to A. actinomycetemcomitans strains ATCC 29523 (serotype a), ATCC 43728 (serotype b) and ATCC 33384 (serotype c). Prevalence (% of positive samples) of A. actinomycetemcomitans was 84.3% in aggressive periodontitis, 60.4% in chronic periodontitis, and 64.0% in periodontally healthy subjects. Proportions of A. actinomycetemcomitans (mean percentage per total bacteria) in periodontally healthy subjects were significantly lower than in aggressive periodontitis subjects. The proportion of serotype b in subjects with aggressive periodontitis and subjects with chronic periodontitis were significantly greater than that in periodontally healthy subjects. The proportion of serotype c in periodontally healthy subjects was much higher than that in chronic periodontitis subjects. The results of this study suggest that prevalence and proportions of A. actinomycetemcomitans are significantly greater in patients with aggressive periodontitis than in those with chronic periodontitis. Serotype b is the predominant serotype of A. actinomycetemcomitans in patients with diseased periodontal conditions. Serotype c is a more common serotype detected in periodontally healthy subjects.

Actinobacillus Infections↗

PubMed2001

Periodontal manifestations of systemic disease.

Periodontitis is a chronic bacterial infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontitis principally through their effects on the normal immune and inflammatory mechanisms. Several conditions may give rise to an increased prevalence, incidence or severity of gingivitis and periodontitis. The effects of a significant number of systemic diseases upon periodontitis are unclear and often it is difficult to causally link such diseases to periodontitis. In many cases the literature is insufficient to make definite statements on links between certain systemic factors and periodontitis and for several conditions only case reports exist whereas in other areas an extensive literature is present. A reduction in number or function of polymorphonuclear leukocytes (PMNs) can result in an increased rate and severity of periodontal destruction. Medications such as phenytoin, nifedipine, and cyclosporin predispose to gingival overgrowth in response to plaque and changes in hormone levels may increase severity of plaque-induced gingival inflammation. Immuno-suppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune mechanisms (such as HIV infection) may predispose the individual to periodontal destruction. There is convincing evidence that smoking has a detrimental effect on periodontal health. The histiocytoses diseases may present as necrotizing ulcerative periodontitis and numerous genetic polymorphisms relevant to inflammatory and immune processes are being evaluated as modifying factors in periodontal disease. Periodontitis severity and prevalence are increased in diabetics and worse in poorly controlled diabetics. Periodontitis may exacerbate diabetes by decreasing glycaemic control. This indicates a degree of synergism between the two diseases. The relative risk of cardiovascular disease is doubled in subjects with periodontal disease. Periodontal and cardiovascular disease share many common risk and socio-economic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying aetiology of both diseases is complex as are the potential mechanisms whereby the diseases may be causally linked. It is thought that the chronic inflammatory and microbial burden in periodontal disease may predispose to cardiovascular disease in ways proposed for other infections such as with Chlamydia pneumoniae. To move from the current association status of both diseases to causality requires much additional evidence. Determining the role a systemic disease plays in the pathogenesis of periodontal disease is very difficult as several obstacles affect the design of the necessary studies. Control groups need to be carefully matched in respect of age, gender, oral hygiene and socio-economic status. Many studies, particularly before the aetiological importance of dental plaque was recognised, failed to include such controls. Longitudinal studies spanning several years are preferable in individuals both with and without systemic disease, due to the time period in which periodontitis will develop.

Calcium Channel Blockers↗

PubMed2001

Systemic and local antimicrobial use in periodontal therapy in England and Wales.

BACKGROUND/AIMS: The aim of this study was to investigate antimicrobial use during periodontal therapy in dental practice in England & Wales. METHOD: This was a postal questionnaire survey of 800 dentists, 400 general dental practitioners (GDP) in National Health Service practice and 400 members of the British Society of Periodontology (Periodontal Society) primarily in dental practice. We designed and piloted a questionnaire to evaluate both systemic and local antibiotic use with periodontal therapy as well as factors affecting their prescription. In addition, we also investigated the potential use of antibiotic sensitivity testing, since this has been recommended prior to prescribing antibiotics. Two follow-up mailings were used to encourage non-responders. RESULTS: The useable return rate for the questionnaires was 587/800 (73%). Systemic antibiotics were used by 7.4% Periodontal Society members and 18.4% GDP for untreated adult periodontitis patients (p<0.001). Antimicrobials were prescribed more frequently by Periodontal Society members in early onset (52.7%) and refractory periodontitis patients (49.6%), and this was highly statistically significantly greater usage than GDP (p<0.001). Regarding local antimicrobials, usage for untreated adult periodontitis was Periodontal Society 8.9% and GDP 5.4%. Higher usage of local antimicrobials was found both for the treatment of recurrent pocketing in adult periodontitis (Periodontal Society 26.3%, GDP 14.8%, p<0.014) and refractory periodontitis (Periodontal Society 30.8%, GDP 15.2%, p<0.001). As reasons for using local antimicrobials, more than 80% of all respondents stated superiority over root debridement alone. Barriers to use included cost, no perceived need and lack of supporting research data. The percentage of responders considering diagnostic microbiology either theoretically or at a cost of pound 60 were by group, Periodontal Society 83% & 70.4% and GDP 76% & 51.2%. 33% of Periodontal Society members and 3.8% of GDP spent at least 45 min per quadrant on root planing and Periodontal Society members had a greater exposure to lectures on both systemic and local drug therapy compared with GDP (p<0.001). CONCLUSIONS: Systemic antimicrobial use was infrequent for adult periodontitis and generally in line with current recommendations for other disease types. Whilst local antimicrobial therapy for periodontitis was not widespread, a substantial minority of dentists use this form of therapy and most believe that it is more effective than root debridement alone.

Adult↗

PubMed1998

Cigarette smoking and periodontal diseases: etiology and management of disease.

Cigarette smoking has long been suspected to be associated with a variety of oral conditions including periodontal diseases. Experimental evidence accumulated over the last 2 decades has indicated that cigarette smoking is probably a true risk factor for periodontitis. This environmental exposure has been associated with 2- to 3-fold increases in the odds of developing clinically detectable periodontitis. Smokers have both increased prevalence and more severe extent of periodontal disease, as well as higher prevalence of tooth loss and edentulism, compared to non-smokers. The greater severity of periodontal destruction may be partly accounted for by the reported increases in the rate of periodontal disease progression. The noxious effect of smoking has been shown to be dose dependent and to be particularly marked in younger individuals; in these subjects, up to 51% of the observed risk of periodontitis was associated with smoking. Much of the literature has also indicated that smokers affected with periodontitis respond less favorably to both non-surgical, surgical, and regenerative periodontal treatments. The success rate of dental implants has also been shown to be compromised in smokers. Furthermore, longterm studies have pointed out that smoking was associated with recurrence of periodontitis during periodontal maintenance; the effect appeared to be dose dependent, with heavy smokers (> 10 cigarettes/day) presenting with higher levels of disease progression. The indication that previous smokers have lower levels of risk for periodontitis compared to current smokers is considered to be the strongest available evidence that smoking cessation will result in improved periodontal health and that smoking cessation counseling should be an integral part of periodontal therapy and prevention. So far, however, no randomized controlled clinical trial establishing the effect of smoking cessation and/or reduction on the periodontal outcomes has been reported. Given the present state of uncertainty about the periodontal benefits, but in light of the established general health gains for the patient that could be derived from a smoking cessation program, practitioners are incorporating smoking cessation counseling as an integral part of periodontal therapy. Furthermore, smoking status represents a key parameter to assess the periodontal risk of an individual subject and therefore to make evidence-based clinical decisions.

Health Education, Dental↗

PubMed2000

Sulfate-reducing bacteria in association with human periodontitis.

BACKGROUND, AIMS: Sulfate-reducing bacteria (SRB) may be etiologically involved in destructive periodontal diseases. These strictly anaerobic bacteria utilize fermentation products for energy conservation by reduction of sulfate to sulfide. This toxic product can accumulate in periodontal pockets in concentrations causing cellular destruction. SRB depend on an actively degrading microbiota to produce a reduced environment, fermentation products and sulfate. The detection frequency of these bacteria is strongly increased in periodontitis compared with healthy sites in the oral cavity. METHOD: In this study, the presence of SRB was determined in relation to clinical features of the patients and to site-specific clinical parameters of periodontitis, such as pocket depth, bleeding and attachment level. Patients with clinical characteristics of severe periodontitis (n=87) were included in the study, 78 were untreated patients and 9 patients were in maintenance care after treatment. Samples were taken (n=261) from the deepest periodontal pockets, and presence of SRB was determined by enrichment culture in an anoxic chamber. RESULTS: In 64% of the patients, SRB were present in at least 1 pocket. They occurred among patients from 23 to 57 years old, and tended to prevail among patients older than 30 years. There was a tendency to increased SRB occurrence among patients with more than 50% of bleeding sites, or with several angular bony defects or furcations. In 44% of the periodontal pockets SRB were present. They tended to prevail in pockets showing bleeding on probing, furcations, angular bony defects, or an endodontal complication. Presence of SRB was positively correlated with increased pocket depth (p<0.05). SRB were found to be associated with various clinical categories of periodontitis, including early onset periodontitis, rapidly progressive periodontitis, adult periodontitis, and refractory periodontitis. Although SRB predominated among patients with an adult form of periodontitis, i.e., with an occurrence of 72%, there was no significant correlation with age of the patient. Among treated patients under maintenance care, SRB prevalence was significantly reduced in comparison with untreated patients (p<0.02). Occurrence of SRB in periodontal pockets showed an odds ratio of 11.2 in comparison with healthy oral sites. CONCLUSION: Periodontal sulfate-reducing bacteria are associated with several clinical categories of periodontitis and with periodontal sites of increased pocket depth.

Adult↗

PubMed2004

Plasma antibody levels in periodontitis patients and controls.

BACKGROUND: A major aspect of the adaptive host response in periodontitis is the production of antibodies. Several risk and susceptibility factors for periodontitis, including smoking, age and composition of the subgingival microflora, have also been suggested to influence antibody production. AIM: The present study was conducted to investigate plasma levels of immunoglobulin (Ig) G, A and M antibodies in periodontitis patients of Caucasian European heritage in relation to disease severity, smoking, diagnosis and prevalence of periodontopathogens. METHODS: In this study, 29 patients with severe periodontitis, 51 with moderate periodontitis and 55 controls without periodontal destruction were enrolled. From the total of 80 patients, 18 were diagnosed with aggressive periodontitis and 62 with chronic periodontitis. Total IgG, IgA and IgM as well as IgG isotypes were analyzed in plasma samples. RESULTS: Levels of total IgG, IgA and IgM were not different between patients and controls; however, in periodontitis, higher levels of IgG1 and IgG2 were observed. Smoking appeared to be significantly and inversely related to antibody levels in periodontitis, in particular for total IgG and IgG2. The absence of an elevated total IgG and IgG2 in smoking patients was irrespective of severity, prevalence of periodontal pathogens and diagnosis. The elevation of total IgG and IgG1 and IgG2 in non-smoker periodontitis patients was observed in patients with moderate periodontitis and even greater in patients with severe periodontitis, but was independent whether patients were infected with Actinobacillus actinomycetemcomitans or Porphyromonas gingivalis and independent of diagnosis. Clinically, it was observed that patients who smoked had more periodontal bone loss; the current findings on antibody levels may be one of several mechanisms related to more extensive periodontal breakdown in smoker patients. CONCLUSION: The current study shows that non-smoker periodontitis patients have higher levels of total IgG and IgG2 than smoker periodontitis patients.

Acute Disease↗

PubMed2005

Factors influencing the diagnosis and treatment of periodontal disease by dental practitioners in Victoria.

BACKGROUND: Healthy periodontal tissues are essential to overall dental health. Therefore, the detection and management of periodontal disease is an integral part of general dental practice. The aim of this study was to investigate confidence in diagnosis and management of periodontal disease by general dental practitioners (GDPs), assess if the Dental Practice Board guidelines on periodontal record keeping are being addressed, and, if necessary, try to find ways of improving the periodontal knowledge of GDPs. METHODS: A survey assessing practitioner confidence in diagnosing and treating periodontal disease was sent to a random selection of 550 dental care providers registered with the Dental Practice Board of Victoria. RESULTS: Two hundred and eighty five (51.8 per cent) of questionnaires were returned completed. It was found that 79.7 per cent of the sampled population screened all new patients for periodontal disease. The majority of respondents felt confident to diagnose and treat gingivitis and initial periodontitis. However, only 61.9 per cent felt confident to diagnose aggressive/early onset periodontitis, and many were not confident in treating advanced periodontitis (36.3 per cent) or aggressive periodontitis (51.6 per cent). The majority of dentists reported that they provided most of the non surgical periodontal therapy to their patients, while most surgical treatments were referred to specialist periodontists. Factors deemed to be important in influencing the decision to provide periodontal treatment included level of training and ability to motivate patients to improve oral hygiene. Many responents requested periodontic continuing education (CE) courses be run. CONCLUSIONS: Most of the dentists surveyed were confident to diagnose periodontal disease and to treat the more common presentations of periodontal disease. There is some evidence to suggest that some practitioners are not following the minimum requirements set by the Dental Practice Board of Victoria in relation to periodontal record keeping. The results also indicate a need for more periodontic CE courses in Victoria.

Clinical Competence↗

PubMed2001

Maternal periodontitis and prematurity. Part I: Obstetric outcome of prematurity and growth restriction.

Oral Conditions and Pregnancy (OCAP) is a 5-year prospective study of pregnant women designed to determine whether maternal periodontal disease contributes to the risk for prematurity and growth restriction in the presence of traditional obstetric risk factors. Full-mouth periodontal examinations were conducted at enrollment (prior to 26 weeks gestational age) and again within 48 hours postpartum to assess changes in periodontal status during pregnancy. Maternal periodontal disease status at antepartum, using a 3-level disease classification (health, mild, moderate-severe) as well as incident periodontal disease progression during pregnancy were used as measures of exposures for examining associations with the pregnancy outcomes of preterm birth by gestational age (GA) and birth weight (BW) adjusting for race, age, food stamp eligibility, marital status, previous preterm births, first birth, chorioamnionitis, bacterial vaginosis, and smoking. Interim data from the first 814 deliveries demonstrate that maternal periodontal disease at antepartum and incidence/progression of periodontal disease are significantly associated with a higher prevalence rate of preterm births, BW < 2,500 g, and smaller birth weight for gestational age. For example, among periodontally healthy mothers the unadjusted prevalence of births of GA < 28 weeks was 1.1%. This was higher among mothers with mild periodontal disease (3.5%) and highest among mothers with moderate-severe periodontal disease (11.1%). The adjusted prevalence rates among GA outcomes were significantly different for mothers with mild periodontal disease (n = 566) and moderate-severe disease (n = 45) by pair-wise comparisons to the periodontally healthy reference group (n = 201) at P = 0.017 and P < 0.0001, respectively. A similar pattern was seen for increased prevalence of low birth weight deliveries among mothers with antepartum periodontal disease. For example, there were no births of BW < 1000 g among periodontally healthy mothers, but the adjusted rate was 6.1% and 11.4% for mild and moderate-severe periodontal disease (P = 0.0006 and P < 0.0001), respectively. Periodontal disease incidence/progression during pregnancy was associated with significantly smaller births for gestational age adjusting for race, parity, and baby gender. In summary, the present study, although preliminary in nature, provides evidence that maternal periodontal disease and incident progression are significant contributors to obstetric risk for preterm delivery, low birth weight and low weight for gestational age. These studies underscore the need for further consideration of periodontal disease as a potentially new and modifiable risk for preterm birth and growth restriction.

Adult↗

PubMed1998

PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression.

Diabetes mellitus is a systemic disease that affects more than 12 million people in the United States and represents a risk factor for periodontitis with odds ratios of 2.1 to 3.0. New data support the concept that in diabetes-associated periodontitis, the altered host inflammatory response plays a critical role. We have recently examined the gingival crevicular fluid (GCF) mediator level, monocytic secretion, and clinical presentation of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 non-diabetic patients with various degrees of periodontal health and disease. First, we found that there was an unexpected high level of GCF mediators among the IDDM subjects, even in the gingivitis and mild periodontitis patients. Furthermore, the GCF and monocytic mediator responses were obviously bimodal in distribution with respect to periodontal status. Gingivitis patients and mild periodontitis patients represented one low response group, and the moderate and severe periodontitis subjects the high response group. Accordingly, these 4 periodontal subgroups were pooled to form 2 main groups for analyses--group A (AAP Types I-II) and group B (AAP Types III-IV). Diabetics had significantly higher GCF levels of both PGE2 and IL-1 beta when compared to non-diabetic controls with similar periodontal status. Within the diabetic group, the GCF levels of these inflammatory mediators were almost 2-fold higher in group B subjects when compared to diabetics from group A. Among diabetics, GCF TNF-alpha levels were only marginally detectable and no significant difference was found between group A and group B patients. Insulin-dependent diabetic patients with gingivitis or mild periodontitis (group A) and moderate to severe periodontitis (group B) have abnormal monocytic inflammatory secretion in response to LPS challenge from Porphyromonas gingivalis (P. gingivalis) as compared to non-diabetic periodontal patients. Data suggest that the diabetic state results in a significantly upregulated monocytic secretion of PGE2 (4.2-fold), IL-1 beta (4.4-fold), and TNF-alpha (4.6-fold) when compared to non-diabetic controls. Within diabetics, LPS dose-response curves demonstrated that monocytes from group B patients secreted approximately 3 times more PGE2 and 6.2 times more TNF-alpha than those from group A; however, there was no significant difference in monocytic IL-1 beta secretion between the 2 diabetic groups. This upregulated monocytic trait is thought to exist independently of the presence of severe periodontal disease since, in non-diabetic patients with adult periodontitis, Gram-negative bacterial infections alone are not sufficient to elicit a systemic hyperresponsive monocytic trait. Between group A and group B diabetics, there was no significant difference in metabolic control as expressed by mean level of glycosylated hemoglobin (HbA1c). In conclusion, our data suggest that diabetic patients have exaggerated inflammatory responses when compared to non-diabetic controls. Furthermore, within diabetics, individuals with moderate to severe periodontitis (group B) have significantly elevated monocytic secretion of PGE2 and TNF-alpha upon LPS challenge and significantly higher GCF levels of PGE2 and IL-1 beta when compared to patients with gingivitis or mild periodontal disease (group A). Thus, we suggest that insulin-dependent diabetes mellitus is a significant risk factor for more severe periodontal disease because, as compared to non-diabetics, diabetic subjects react with an abnormally high degree of inflammation to an equivalent bacterial burden.

Adult↗

PubMed2006

Levels of immunoglobulin A1 and messenger RNA for interferon gamma and tumor necrosis factor alpha in total saliva from patients with diabetes mellitus type 2 with chronic periodontal disease.

BACKGROUND: Diabetes mellitus and periodontal disease have high incidence in the general population and are associated with various degrees of dysfunction in the immune system. It has been shown that diabetic patients with severe periodontal disease have more complications of diabetes and less effective metabolic control compared with diabetic patients with healthy gingiva. Patients with diabetes and severe periodontal disease present higher levels of serous immunoglobulin A (IgA). Elevation of the IgA1 isotype is thought to contribute to this phenomenon. Another important event in the diabetes-periodontitis association is the disturbance in local and systemic production of inflammatory cytokines. OBJECTIVE: In this study we tested the hypothesis that type 2 diabetic patients with chronic moderate periodontal disease have differences in salivary IgA1 titers and cytokine expression when compared with the chronic severe periodontal disease cases. METHODS: We utilized a jacalin-IgA capture assay to determine the IgA1 titers in total saliva and reverse transcriptase-polymerase chain reaction to detect mRNA for interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) in total saliva samples of 13 patients with chronic moderate periodontal disease and 10 with chronic severe periodontal disease. RESULTS AND CONCLUSIONS: We observed a predominance of IgA1 titers of 64 (45.5%) in saliva samples from chronic severe periodontal disease patients and titers averaging 512 (30.8%) in chronic moderate periodontal disease patients. We detected mRNA for IFN-gamma in six out of 10 chronic severe periodontal disease subjects and in two out of 13 chronic moderate periodontal disease patients. TNF-alpha expression was similar in both groups. Our data suggest that higher levels of IgA1 may exert partial protection of the periodontal tissue in chronic moderate periodontal disease diabetic patients when compared to severe periodontal disease. Despite the small number of patients, IFN-gamma expression had a trend association with severity of periodontitis and TNF-alpha gene expression did not correlate with severity of periodontal disease.

Artocarpus↗

PubMed1995

Longitudinal assessment of early onset periodontitis.

The purpose of this study was to determine the clinical course of early onset periodontitis and to investigate factors which may influence its clinical course. For the past 15 years we have been conducting a study of families with early onset periodontitis, and have examined 142 localized juvenile periodontitis and 185 severe generalized early onset periodontitis patients. In order to study the clinical course of early onset periodontitis we recalled our subject population to determine their periodontal status. Forty (40) patients with localized early onset periodontitis (LJP) and 48 with generalized early onset periodontitis (SP) were re-examined. The time since the most recent visit for LJP patients was approximately 3 years and for SP patients almost 4 years. LJP patients who received periodontal therapy on the average gained periodontal attachment. In contrast, LJP patients who did not receive therapy lost periodontal attachment. SP patients lost periodontal attachment regardless of whether or not they had periodontal therapy. SP patients also lost an average of one tooth during the approximately 4 years of observation. LJP patients lost very few teeth with only 4 teeth being lost in 40 patients. The results of this study suggest that localized juvenile periodontitis is a stable disease in most individuals. In contrast, patients with severe generalized early onset periodontitis continued to lose both periodontal attachment and teeth.

Adult↗

PubMed2001

Periodontal risk assessment, diagnosis and treatment planning.

The prevention and treatment of the periodontal diseases is based on accurate diagnosis, reduction or elimination of causative agents, risk management and correction of the harmful effects of disease. Prominent and confirmed risk factors or risk predictors for periodontitis in adults include smoking, diabetes, race, P. gingivalis, P. intermedia, low education, infrequent dental attendance and genetic influences. Several other specific periodontal bacteria, herpesviruses, increased age, male, sex, depression, race, traumatic occlusion and female osteoporosis in the presence of heavy dental calculus have been shown to be associated with loss of periodontal support and can be considered to be risk indicators of periodontitis. The presence of furcation involvement, tooth mobility, and a parafunctional habit without the use of a biteguard are associated with a poorer periodontal prognosis following periodontal therapy. An accurate diagnosis can only be made by a thorough evaluation of data that have been systematically collected by: 1) patient interview, 2) medical consultation as indicated, 3) clinical periodontal examination, 4) radiographic examination, and 5) laboratory tests as needed. Clinical signs of periodontal disease such as pocket depth, loss of clinical attachment and bone loss are cumulative measures of past disease. They do not provide the dentist with a current assessment of disease activity. In an attempt to improve the ability to predict future disease progression, several types of diagnostic tests have been studied, including host inflammatory products and mediators, enzymes, tissue breakdown products and subgingival temperature. In general, the usefulness of these tests for predicting future disease activity remains to be established in terms of sensitivity, specificity and predictive value. Although microbiological analysis of subgingival plaque is not necessary to diagnose and treat most patients with periodontitis, it is helpful when treating patients with unusual forms of periodontal disease such as early-onset, refractory and rapidly progressive disease. There appears to be a strong genetic component in some types of periodontal disease and genetic testing for disease susceptibility has potential for future use, but more research is needed to determine its utility for use in clinical practice. Treatment of the periodontal diseases may be divided into four phases: systemic, hygienic, corrective and maintenance or supportive periodontal therapy. Regardless of the type of treatment provided, periodontal therapy will fail or will be less effective in the absence of adequate supportive periodontal therapy.

Bacteriological Techniques↗

PubMed1983

Suppression of the periodontopathic microflora in localized juvenile periodontitis by systemic tetracycline.

Since recent studies have implicated Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis, this investigation determined the effectiveness of subgingival debridement, topical Betadine Solution, and systemic tetracycline in suppressing subgingival A. actinomycetemcomitans and other microorganisms. A total of 20 deep periodontal pockets and 10 normal periodontal sites of 6 localized juvenile periodontitis patients was included in the study. Each patient was treated in 3 stages over a period of 22 weeks, and the result of treatment was monitored for an additional 38 weeks. The first stage of treatment included plaque control, as well as thorough scaling and root planing, composed of at least 6 h of debridement. No concomitant periodontal surgery was performed. In the second stage, Betadine saturated cotton gauze was inserted into the periodontal pockets for 10 min. Stage 3 involved systemic tetracycline therapy (1 g/day) for 14 days. The subgingival microflora was determined at frequent intervals by selective culturing of A. actinomycetemcomitans and Capnocytophaga and by direct microscopic examination. The clinical effect was assessed by measuring changes in probing periodontal attachment level, probing periodontal pocket depth, radiographic alveolar bone mass, and other relevant clinical parameters. Scaling and root planing reduced the total subgingival bacterial counts and the proportions of certain Gram-negative bacteria, but no periodontal pocket became free of A. actinomycetemcomitans. Betadine application had little or no effect on the subgingival microflora. In contrast, tetracycline administered via the systemic route suppressed A. actinomycetemcomitans, Capnocytophaga, and spirochetes to low or undetectable levels in all test periodontal pockets. A. actinomycetemcomitans reappeared in 9 of the deep periodontal pockets after the administration of tetracycline. Most of these 9 pockets became free of detectable A. actinomycetemcomitans during the second week of tetracycline administration, whereas pockets which yielded no A. actinomycetemcomitans after tetracycline therapy became free of the organisms during the first week of tetracycline treatment. This data suggests that systemic tetracycline therapy of localized juvenile periodontitis should, as a practical rule, be continued for 3 weeks. Periodontal destruction continued in 4 deep pockets which all showed high posttetracycline A. actinomycetemcomitans counts. All 6 pockets which demonstrated a marked gain in periodontal attachment yielded no cultivable A. actinomycetemcomitans. No association was found between periodontal disease status and subgingival Capnocytophaga, spirochetes or motile rods. The present study indicates that A. actinomycetemcomitans is an important etiologic agent in localized juvenile periodontitis.(ABSTRACT TRUNCATED AT 400 WORDS)

Actinobacillus↗

PubMed1997

Is the chemical prevention of gingivitis necessary to prevent severe periodontitis?

Gingival inflammation seldom causes discomfort, social embarrassment or loss of function. As most sites with gingival inflammation do not progress to severe periodontal disease, gingivitis should not be considered a public health problem. Periodontitis is always preceded by gingivitis. But most gingivitis remains stable for years without progressing to periodontitis. The number of gingivitis sites that do convert is small. The levels of oral cleanliness achieved by the majority of populations in industrialized countries are below the threshold for severe destructive periodontal disease of personal and public health concern. Because methods of measuring the progression of periodontal disease are unreliable, definitive answers regarding conversion of gingivitis to severe periodontitis are lacking. Gingival inflammation frequently remains contained; most gingivitis remains stable for years without progressing to periodontitis. Decreasing gingivitis does reduce shallow pocketing, but the effect on severe periodontitis is not clear. Although the underlying justification for the reduction of plaque is to reduce gingival inflammation to prevent or reduce severe periodontitis and tooth loss, the basis for the approach is equivocal. A reasonably high level of plaque appears to be compatible with acceptably low levels of periodontal disease. Reducing nonspecific plaque levels to such levels is therefore a rational goal. The conventional methods of controlling periodontal disease involve mechanical removal of plaque and calculus. A complimentary ecological approach, using chemicals, would be to alter the environment of the pocket to prevent growth of putative pathogens. Any ecological approach should be sensitive to the dangers of disrupting the natural ecology of dental plaque. Some antimicrobial and antimetabolic agents such as fluoride, chlorhexidine and triclosan and zinc citrate can selectively suppress certain organisms or inhibit bacterial proteases implicated in tissue damage. The uncertainties about factors that convert gingival inflammation into periodontitis and periodontitis into severe periodontitis coupled with insufficient data from controlled clinical trials on the effectiveness of chemical reduction of gingivitis to prevent severe periodontitis leads one to conclude that more research is required before the need for the chemical prevention of gingivitis to prevent severe periodontitis can be justified.

Dental Plaque↗

PubMed2001

Periodontal infections contribute to elevated systemic C-reactive protein level.

BACKGROUND: Periodontitis is a local inflammatory process mediating destruction of periodontal tissues triggered by bacterial insult. However, this disease is also characterized by systemic inflammatory host responses that may contribute, in part, to the recently reported higher risk for cardiovascular disease (CVD) among patients with periodontitis. Moderate elevation of C-reactive protein (CRP) has been found to be a predictor of increased risk for CVD. Elevated CRP levels in periodontal patients have been reported by several groups. In this study, we examined whether CRP plasma levels are increased in periodontitis and if there is a relation to severity of periodontal disease and to the periodontal microflora. METHODS: CRP serum levels were assessed using radial immunodiffusion assay in 174 subjects, 59 with moderate mean clinical attachment loss (AL) (2.39+/-0.29 mm) and 50 with high AL (3.79+/-0.86 mm) as compared to 65 periodontally healthy controls (AL, 1.74+/-0.18 mm). Clinical attachment loss, probing depths, and percentage of periodontal pocket sites > or =5 mm were measured. The presence of periodontal pathogens Porphyromonas gingivalis (P.g.), Prevotella intermedia (P.i.), Campylobacter recta (C.r.), and Bacteroides forsythus (B.f.) in subgingival plaque samples was measured by immunofluorescence microscopy. RESULTS: Statistically significant increases in CRP levels were observed in subjects with periodontal disease when compared to healthy controls (P= 0.036). Subjects with high levels of mean clinical attachment loss had significantly higher mean CRP levels (4.06+/-5.55 mg/l) than controls (1.70+/-1.91 mg/l), P= 0.011. The CRP levels were adjusted for factors known to be associated with elevated CRP, including age, smoking, body mass index (BMI), triglycerides, and cholesterol. Age and BMI were found to be significant covariates. The reported range for CRP as a risk factor for CVD, peripheral vascular diseases, or stroke is 1.34 mg/l to 6.45 mg/l and the mean of this range is 3 mg/l. The percentage of subjects with elevated levels of CRP > or = 3 mm was significantly higher in the high clinical AL group (38%; 95% Cl: 26.7%, 49.3%) when compared to the control group (16.9%; 95% CI: 9.25%, 24.5%), P= 0.011. The presence of periodontal pathogens P.g., P.i., C.r., and B.f. in subgingival samples was positively associated with elevated CRP levels (P= 0.029). CONCLUSIONS: The extent of increase in CRP levels in periodontitis patients depends on the severity of the disease after adjusting for age, smoking, body mass index, triglycerides, and cholesterol. Also, there are elevated levels of CRP associated with infection with subgingival organisms often associated with periodontal disease, including P.g., P.i., C.r., and B.f. Recent investigations emphasized the role of moderate elevated CRP plasma levels as a risk factor for CVD. The positive correlation between CRP and periodontal disease might be a possible underlying pathway in the association between periodontal disease and the observed higher risk for CVD in these patients.

Adult↗

PubMed1986

Juvenile periodontitis.

Juvenile periodontitis occurs in children and young adults and can be classified into: periodontitis which occurs in otherwise healthy individuals, and periodontitis which occurs in juveniles with systemic disease. The periodontitis which occurs in otherwise healthy individuals consists of two major forms: juvenile periodontitis, also called periodontosis or localized juvenile periodontitis (LJP), and generalized juvenile periodontitis which includes early onset adult periodontitis, recurrent necrotizing ulcerative periodontitis and the true generalized form of juvenile periodontitis. Periodontitis in systemically diseased individuals can be divided into three subgroups: juvenile periodontitis associated with primary neutrophil disorders, juvenile periodontal disease in which neutrophils are secondarily abnormal, and juvenile periodontitis associated with other diseases. Juvenile periodontitis is perhaps the best understood form of periodontal disease. A major infecting organism, Actinobacillus actinomycetemcomitans, is strongly associated with the disease, and may be an exogenous pathogen since it is not found in healthy individuals or in healthy sites in LJP patients. It is virulent with marked leukaggressive properties and it induces a marked antibody response in infected patients. Eradication of Actinobacillus actinomycetemcomitans requires attention to the fact that it invades the tissue and hence systemic antimicrobials or surgical excision of the tissues is necessary for eradication. Marked suppression of the organism from subgingival sites is associated with healing. Host responses in LJP have also been well described and most immune functions studied appear to be normal. The notable exception is neutrophil chemotaxis which is depressed. Associated with depressed neutrophil chemotaxis is a reduction of neutrophil receptors for several chemotactic factors including C5a, the fifth component of complement.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗