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PubMed1997

Tooth loss due to periodontal abscess: a retrospective study.

This retrospective study focused on the frequency of tooth loss due to periodontal abscess among 42 patients who were treated by a single clinician over a 5- to 29-year period. A total of 114 patients were selected from the active periodontal recall schedule of a single periodontist at The University of Iowa College of Dentistry. The criteria for inclusion in the study included having a history of moderate to advanced periodontitis, being on 3 to 6 month recall periodontal maintenance care, and completion of active periodontal therapy prior to October 1987. Other parameters evaluated were age; gender; number of teeth present and missing at the initial, reevaluation, and last periodontal recall visit; initial periodontal prognosis; furcation involvement; non-surgical and surgical periodontal therapy; and reasons for tooth loss. Patients were grouped according to the number of teeth lost following active periodontal treatment into well-maintained (0 to 3), downhill (4 to 9), and extreme downhill (10 to 23) groups. Forty-two of the 114 patients were identified as having one or more periodontal abscesses. A total of 109 teeth were affected by periodontal abscess of which 49 (45%) teeth were lost and 60 (55%) were successfully maintained over an average of 12.5 years (5 to 29 years). More furcated teeth were lost than nonfurcated teeth and teeth given a hopeless prognosis were lost more consistently than those given a questionable prognosis in all groups. The frequency of periodontal abscess and tooth loss per patient was greater in the downhill and extreme downhill response groups than the well-maintained group. This suggests that teeth with a history of periodontal abscess can be treated and maintained for several years.

Female↗

PubMed2003

The effect of enamel matrix proteins on periodontal regeneration as determined by histological analyses.

BACKGROUND: Therapeutic approaches to periodontal regeneration in the past have utilized bone replacement grafts, growth factors, barrier membranes, or combinations of these approaches. More recently, enamel extracellular matrix proteins have been introduced to stimulate periodontal regeneration. One factor thought to have an impact on the outcome of the regenerative process is the initial size of the periodontal defect. This is particularly the case when using proteins to stimulate regeneration, because the concepts of guided tissue regeneration emphasize the need for space maintenance to allow for selected cell repopulation. The goal of this study was to evaluate periodontal regeneration in intrabony defects of various sizes treated with enamel matrix proteins. METHODS: Periodontal defects ranging in size from 1 to 6 mm were created bilaterally around 3 teeth in the mandibles of baboons. Plaque was allowed to accumulate around ligatures placed into the defects. After 2 months, the ligatures were removed, the teeth were scaled and root planed, and a notch was placed at the base of the defect. On one side of the mandible, neutral ethylene diamine tetracetic acid and enamel matrix proteins were used to treat the defects. The other side served as a control, with neutral ethylene diamine tetracetic acid treatment alone after scaling and root planing. Flaps were sutured and the animals were allowed to heal without oral hygiene procedures. After 5 months, the animals were sacrificed and the teeth were processed for histological evaluation. RESULTS: Periodontal regeneration occurred in all sizes of the periodontal defects. Qualitatively, new cementum, periodontal ligament with Sharpey's fibers, and new bone tissue were observed. In general, enamel matrix protein treatment resulted in greater tissue formation than controls. In many instances, dramatic tissue formation occurred far coronal to the base of the defects. In addition, horizontal bone fill occurred in defects that were initially 4 or 6 mm wide. The resultant width of the periodontal ligament was similar in all defects regardless of the original defect width. The cementum width was slightly greater in the wider (4 and 6 mm) defects compared to the more narrow (1 and 2 mm) defects. When evaluating the combined 1 and 2 mm defects, the height of new cementum with enamel matrix protein treatment was 45% greater than the control, with 31% greater new bone height versus the control. In the combined wider defects (4 and 6 mm), new tissue height was more similar between enamel matrix protein-treated defects and control defects. The results from the wider defects must be interpreted cautiously, because the interproximal bone heights were resorbed more adjacent to the wider defects during the plaque accumulation period and likely limited the potential for regeneration. CONCLUSIONS: The treatment of various sized periodontal defects with enamel matrix proteins stimulated substantial periodontal regeneration. In many cases, dramatic amounts of new cementum, Sharpey's fibers, periodontal ligament, and bone tissue were formed far coronal to the notch at the base of the defect, especially considering the width of the original defects. This periodontal regeneration occurred in the absence of exogenous growth factors, bone replacement grafts, barrier membranes, or their combination.

Alveolar Bone Loss↗

PubMed2004

Total proteoglycan and chondroitin-4-sulfate levels in gingiva of patients with various types of periodontitis.

BACKGROUND: The aim of the present study was to investigate the total proteoglycan (PG) and chondroitin-4-sulfate (C4S) levels in gingival tissue samples obtained from patients with aggressive periodontitis (AgP) and chronic periodontitis (CP) before therapy (baseline) and 1 month after completion of non-surgical periodontal therapy. METHODS: Gingival tissue samples were obtained from 10 AgP and 10 CP patients before initiation of treatment (baseline) and 1 month after non-surgical periodontal treatment. The control group comprised 10 systemically and periodontally healthy subjects. Total PG and C4S levels were determined by biochemical techniques. PG levels were analyzed using a modified Bitter and Muir method. C4S assay was carried out using chondroitin sulphate lyase AC and chondroitin-6 sulphate sulphohydrolase enzymes. The results were tested statistically using parametric tests. RESULTS: The clinical periodontal parameters demonstrated significant decreases in the periodontitis groups (P<0.05) after treatment, and there was no significant difference between AgP and CP groups at baseline and after treatment (P>0.05). At baseline, total PG and C4S levels in both of the periodontitis groups were significantly lower than that of the control group (P<0.05). One month after the non-surgical periodontal treatment, total PG levels in the periodontitis groups were comparable to the control group (P>0.05), whereas C4S levels in the AgP group were significantly lower than the other study groups (P<0.05). In the CP group, total PG and C4S levels increased significantly (P = 0.001 and P = 0.006, respectively) after non-surgical periodontal treatment, but they did not increase in the AgP group (P>0.05). CONCLUSION: The significant increases observed in total proteoglycan and chondroitin-4-sulfate levels after non-surgical periodontal treatment in the CP group but not in the AgP group may suggest that healing patterns differ between the two periodontitis types in terms of PG and C4S composition of extracellular matrix.

Adult↗

PubMed2001

Subgingival microflora and antibody responses against periodontal bacteria of young Japanese patients with type 1 diabetes mellitus.

Periodontal disease is a complication of patients with type 1 diabetes mellitus (T1DM), although the mechanisms responsible for this relationship remain unclear. The aim of this study was to examine oral manifestations and the prevalence of periodontal pathogens from subgingival plaque samples and serum IgG antibody levels against them in young Japanese type 1 diabetic subjects. One hundred and seventeen Japanese T1DM subjects (53 male, 64 female, mean age +/- SD, 16 +/- 6.5 years) participated in this study. Thirty-nine periodontally healthy, age-matched nondiabetics served as controls. T1DM subjects were clinically assigned into three groups: 12 periodontitis, 32 gingivitis and 73 periodontally healthy. Microbiological tests for four periodontal pathogens, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia and Capnocytophaga ochracea were performed using 16S ribosomal RNA-based polymerase chain reaction methods. Serum IgG antibody levels against 12 periodontal bacteria including the four species assessed by polymerase chain reaction were measured by enzyme-linked immunosorbent assay. In the T1DM subjects, the Periodontitis group had a significantly longer mean duration of diabetes and a higher percentages of subjects harbouring P. gingivalis and P. intermedia than the Periodontally Healthy group. Serum IgG antibody levels against P. gingivalis were significantly elevated in the Periodontitis group compared with Gingivitis and Periodontally Healthy groups. These results indicate that Japanese T1DM subjects are a high-risk group for periodontal disease and both P. gingivalis infection and duration of T1DM are risk factors for the progression of periodontitis in patients with T1DM.

Adolescent↗

PubMed2004

[The stages of comprehensive periodontal therapy--diagnosis-driven treatment planning].

The rationale and the stages of the comprehensive periodontal treatment are overviewed. The consecutive phases are logically following each other. Basically three major therapeutical categories can be established, such as: 1. absolutely healthy from periodontal point of view, 2. gingivitis, 3. periodontitis. Within the periodontitis group the basic principles and strategies are totally different for the management of chronic and aggressive periodontitis cases. Principally the comprehensive periodontal therapy can be divided into four main phases: phase I. initial or cause related therapy, phase II. surgical therapy, phase III. periodontal reconstruction, and phase IV. periodontal maintenance. The classic non-surgical and surgical techniques can cure inflammation, arrest the progression of periodontal destruction and restore gingival-periodontal health, and the outcome is quite predictable for gingivitis and chronic periodontitis. The long-lasting results are dependent on the patients' motivation and maintenance. The late therapeutical results and the maintenance of aggressive periodontitis cases are less predictable. Technically the vertical component of the bone loss can be fully corrected by regenerative surgical techniques. So far the horizontal bone loss should be considered as an irreversible feature as no periodontal regenerative techniques are available to restore the lost alveolar crest and interdental septa.

Chronic Disease↗

PubMed2004

[Interleukin-1beta and IL-1 receptor antagonist levels in gingival crevicular fluid and their relationship to clinical indices of periodontitis].

OBJECTIVE: To investigate Interleukin-1beta (IL-1beta) and IL-1 receptor antagonist (IL-1ra) concentrations in gingival crevicular fluid (GCF) of periodontally healthy teeth and to periodontitis teeth and to reveal their relationships to periodontal clinical indices. METHODS: Thirty GCF samples were harvested from periodontally healthy sites in which 15 samples were from periodontally healthy subjects and 15 GCF samples were from patients with chronic periodontitis, and 43 GCF samples (including 28 samples from BOP positive sites and 15 samples from BOP negative sites) were harvested from periodontitis sites of 33 patients with chronic periodontitis. Clinical indices (GI, PPD and CAL) were recorded for each tooth. The concentrations of IL-1beta and IL-1ra in GCF were quantified by ELISA method. RESULTS: (1) The mean concentrations of IL-1beta and IL-1ra and the average value of 10(4)IL-1beta/IL-1ra for periodontally healthy teeth were (61.891 +/- 20.719) pg/ml, (739.410 +/- 249.121) ng/ml and 0.857 +/- 0.375, respectively. The mean concentration of IL-1beta (224.402 +/- 87.416) pg/ml and the average value of 10(4)IL-1beta/IL-1ra for periodontitis teeth 6.813 +/- 0.375 were greater than those for healthy teeth, respectively (P<0.0001), and in contrast, the mean concentration of IL-1ra for periodontitis teeth (366.722 +/- 104.188) ng/ml was lower than that for healthy sites(P<0.0001). (2) For all sites, a strong inverse relationship was found between IL-1beta and IL-1ra levels in GCF (P<0.01). Both of IL-1beta and 10(4) IL-1beta/IL-1ra values had positive correlations with GI, PPD and CAL (P<0.01). And the negative correlation was found between GI and IL-1ra (P<0.05). (3) The mean concentration of IL-1beta and the average value of 10(4)IL-1beta/IL-1ra at BOP positive teeth were greater than those at BOP negative teeth (P<0.0001), and the mean concentration of IL-1ra at BOP positive teeth was lower than that at BOP negative teeth (P<0.01). CONCLUSION: The results suggest that the increasing GCF level of IL-1beta and decreasing level of IL-1ra may be an important factor for the pathogenesis and development of chronic periodontitis and IL-1ra has an inhibitory effect on IL-1beta activity. The GCF level of IL-1beta and the value of 10(4)IL-1beta/IL-1ra, especially the latter one, are closely associated with the clinical indices of chronic periodontitis.

Adult↗

PubMed2004

[Periodontal abscess: etiology, diagnosis and treatment].

The periodontal abscess is an acute destructive process in the periodontium resulting in localized collections of pus communicating with the oral cavity through the gingival sulcus or other periodontal sites and not arising from the tooth pulp. The prevalence of periodontal abscess is relatively high and it affects the prognosis of the tooth. Periodontal abscesses can develop on the base of persisting periodontitis but can also occur in the absence of periodontitis. The cause of the development of periodontal abscess originating from chronic periodontitis is the marginal closure of a periodontal pocket, or the pocket lumen might be too tight to drain the increased suppuration due to changes in the composition of subgingival microflora, alteration of bacterial virulence or host defenses. Diagnosis of a periodontal abscess is based on medical and dental history as well as oral examination (pocket depth, swelling, suppuration, mobility, sensibility of the tooth). The most prevalent group of bacteria: P. gingivalis, P. intermedia, B. forsythus, F. nucleatum and P. micros. Previous studies have suggested that the complete therapy of the periodontitis patients with acute periodontal abscess has to do in two stages: the first stage is the management of acute lesions, then the second stage is the appropriate comprehensive treatment of the original and/or residual lesions. The management of acute lesions includes establishing drainage via pocket lumen, subgingival scaling and root planing, curettage of the lining pocket epithelia and seriously inflamed connective tissue, compressing pocket wall to underlying tooth and periodontal support, and maintaining tissue contact. Some authors recommend the incision or to establish drainage and irrigation, or a flap surgery, or even extraction of hopeless teeth. We recommend the use of systemic antibiotics as a preventive measure of systemic disease or in case of systemic symptoms.

Acute Disease↗

PubMed2005

Tobacco smoking and periodontal health in a Saudi Arabian population.

BACKGROUND & AIM: Tobacco smoking exerts a harmful effect on the periodontal tissues manifested by periodontal pockets, attachment loss and periodontal bone loss. Current evidences on the effects of tobacco on periodontal health mainly concern cigarette smoking. In view of the increasing popularity of water pipe smoking in Arabian countries and reports confirming that water pipe smoking has health effects similar to those of cigarette smoking, there is a need for a better understanding of the potential harm of this smoking habit. The present thesis was carried out in order to explore whether water pipe smoking is associated with periodontal health in a manner similar to cigarette smoking. MATERIAL & METHODS: Residents in Jeddah City, Saudi Arabia, were invited to participate in the study by means of announcements in two daily newspapers. 355 individuals, 100 women and 255 men (17-60 years) responded to a standardized questionnaire and digital panoramic dental radiographs were taken. The questionnaire included information about oral hygiene practices, dental care and smoking habits. Of these subjects, 262 (73%) also volunteered for clinical examination, including assessments of oral hygiene, gingival inflammation and probing depth. Subgingival microbial test was carried out in 198 individuals for the detection of 12 different bacterial species most commonly associated with periodontal disease using the checkerboard DNA-DNA hybridization technique. Participants were stratified into water pipe smokers 33%, cigarette smokers 20%, smokers of both water pipe and cigarettes (mixed smokers 19%) and non-smokers 28%. RESULTS: Tobacco smoking is associated with a suppression of the gingival bleeding response to plaque accumulation. A suppressive effect was observed in both cigarette and water pipe smokers compared to non-smokers (Study I). Both cigarette and water pipe smoking were associated with the presence of more than 10 pockets of > or = 5 mm probing depth. The relative risk for periodontal disease was 5.1-fold and 3.8-fold increased in water pipe and cigarette smokers, respectively, compared to non-smokers (p < 0.01). The relative risk associated with heavy smoking was about 8-fold elevated in water pipe smokers and 5-fold elevated in cigarette smokers, suggesting an exposure-response effect (Study II). Tobacco smoking was associated with a reduction of the periodontal bone height. The reduction was of similar magnitude in water pipe smokers and cigarette smokers. The relative risk of periodontal bone loss of more than 30% of the root length was 3.5-fold and 4.3-fold elevated in water pipe and cigarette smokers, respectively, compared to non-smokers (p < 0.01). The relative risk associated with heavy smoking was 7.5-fold elevated in water pipe smokers and 6.3-fold elevated cigarette smokers (Study III). Further more, cigarette smokers, water pipe smokers and non-smokers exhibited similar periodontal microflora (Study IV). CONCLUSION: Tobacco smoking is associated with inferior periodontal health. The impact of water pipe smoking is of largely the same magnitude as that of cigarette smoking. The association between tobacco smoking and an inferior periodontal health seems to be independent of the subgingival microflora. Water pipe smoking habit should be considered in periodontal health.

Adolescent↗

PubMed2000

Cigar, pipe, and cigarette smoking as risk factors for periodontal disease and tooth loss.

BACKGROUND: Our purpose was to test the hypotheses that cigar and pipe smoking have significant associations with periodontal disease and cigar, pipe, and cigarette smoking is associated with tooth loss. We also investigated whether a history of smoking habits cessation may affect the risk of periodontal disease and tooth loss. METHODS: A group of 705 individuals (21 to 92 years-old) who were among volunteer participants in the ongoing Baltimore Longitudinal Study of Aging were examined clinically to assess their periodontal status and tooth loss. A structured interview was used to assess the participants' smoking behaviors with regard to cigarettes, cigar, and pipe smoking status. For a given tobacco product, current smokers were defined as individuals who at the time of examination continued to smoke daily. Former heavy smokers were defined as individuals who have smoked daily for 10 or more years and who had quit smoking. Non-smokers included individuals with a previous history of smoking for less than 10 years or no history of smoking. RESULTS: Cigarette and cigar/pipe smokers had a higher prevalence of moderate and severe periodontitis and higher prevalence and extent of attachment loss and gingival recession than non-smokers, suggesting poorer periodontal health in smokers. In addition, smokers had less gingival bleeding and higher number of missing teeth than non-smokers. Current cigarette smokers had the highest prevalence of moderate and severe periodontitis (25.7%) compared to former cigarette smokers (20.2%), and non-smokers (13.1%). The estimated prevalence of moderate and severe periodontitis in current or former cigar/pipe smokers was 17.6%. A similar pattern was seen for other periodontal measurements including the percentages of teeth with > or = 5 mm attachment loss and probing depth, > or = 3 mm gingival recession, and dental calculus. Current, former, and non- cigarette smokers had 5.1, 3.9, and 2.8 missing teeth, respectively. Cigar/pipe smokers had on average 4 missing teeth. Multiple regression analysis also showed that current tobacco smokers may have increased risks of having moderate and severe periodontitis than former smokers. However, smoking behaviors explained only small percentages (<5%) of the variances in the multivariate models. CONCLUSION: The results suggest that cigar and pipe smoking may have similar adverse effects on periodontal health and tooth loss as cigarette smoking. Smoking cessation efforts should be considered as a means of improving periodontal health and reducing tooth loss in heavy smokers of cigarettes, cigars, and pipes with periodontal disease.

Adult↗

PubMed2001

Treponema socranskii, Treponema denticola, and Porphyromonas gingivalis are associated with severity of periodontal tissue destruction.

BACKGROUND: The aim of the present study was to identify Treponema socranskii in addition to Treponema denticola and Porphyromonas gingivalis by polymerase chain reaction (PCR), and to clarify the relationship between the presence of these microorganisms and the severity of clinical periodontal parameters. METHODS: Saliva and subgingival plaque collected from 123 subjects (38 aggressive periodontitis patients, 65 chronic periodontitis patients, 20 healthy patients) were subjected to PCR to detect the aforementioned 3 microorganisms. RESULTS: Detection frequencies of T. socranskii, T. denticola, and P. gingivalis in plaque samples from aggressive periodontitis patients (71.1%, 73.7%, 84.2%, respectively) and chronic periodontitis patients (89.2%, 93.8%, 95.3%) were much higher than those from healthy subjects (30%, 5.0%, 10.0%). In aggressive and chronic periodontitis patients, these 3 species of bacteria were detected frequently at sites that showed deep periodontal pockets and severe attachment loss. The percentage of these bacteria-positive sites increased as the gingival index score of chronic periodontitis patients increased. T. socranskii was frequently detected together with T. denticola or P. gingivalis at the same sites, and coexistence of these microorganisms was frequently observed in deep periodontal pockets of aggressive periodontitis patients. CONCLUSIONS: T. socranskii, T. denticola, and P. gingivalis were frequently detected in periodontitis patients by PCR. The prevalence of these 3 microorganisms was correlated with various clinical parameters. Taken together, our findings suggest that T. socranskii, T. denticola, and P. gingivalis are associated with the severity of periodontal tissue destruction.

Adolescent↗

PubMed2002

Subgingival microbial profiles in refractory periodontal disease.

BACKGROUND/AIM: The purpose of the present investigation was to examine subgingival microbial profiles associated with refractory periodontitis and to seek such profiles in periodontally healthy, periodontally well-maintained elder and untreated periodontitis subjects. METHODS: 36 subjects were defined as refractory on the basis of further attachment loss after scaling and root planing, surgery and systemically administered antibiotics. A total of 890 subgingival plaque samples (mean/subject=24.7) were taken from the mesial aspect of each tooth in each subject at baseline and individually processed for their content of 40 subgingival taxa using checkerboard DNA-DNA hybridization. Cluster analysis was performed on mean within subject species counts using the chord coefficient and an average unweighted linkage sort. Significant differences among clusters for individual and complexes of species were sought using the Kruskal Wallis test. The microbial profiles of the refractory subjects were compared with those of 27 periodontally healthy subjects (n plaque samples=708), 35 periodontally well-maintained elder subjects (n plaque samples=801) and 115 untreated adult periodontitis subjects (n plaque samples=2871). RESULTS: 28 of 36 refractory subjects fell into 4 clusters with >29% similarity. 10 of 40 species and 4 of 7 complexes differed significantly among clusters. Profile (Cluster) I (n=4) was characterized by high proportions of "yellow" and "green" complex species, profile II (n=3) by low total counts and high proportions of "orange" and "purple" complex species, profile III (n=9) by high total counts and counts of Actinomyces and "purple" complex species, profile IV (n=12) by high proportions of "red" and "orange" complex species. The mean profiles of each cluster were subjected to cluster analysis with microbial data from 4380 (mean 24.7) baseline subgingival plaque samples from 27 periodontally healthy, 35 treated, well-maintained elders and 115 untreated adult periodontitis subjects. 12 clusters were formed with >41% similarity. 3 of the refractory profiles were detected in 3 cluster groups. Profile II in a cluster of 1 healthy, 1 elder and 4 untreated periodontitis subjects; profile III in a cluster of 1 healthy, 2 elder and 12 periodontitis subjects; Profile IV, with 1 healthy and 5 untreated periodontitis subjects. The profile not detected in non refractory subjects was dominated by Streptococcus species. 9 clusters did not harbor refractory profiles. 11.1% of healthy, 8.6% of elder and 18.3% of periodontitis subjects were in clusters exhibiting refractory microbial profiles. CONCLUSIONS: 4 subgingival microbial profiles were detected among refractory subjects. "Refractory microbial profiles" could be detected in subjects who had not yet exhibited refractory disease.

Actinobacillus↗

PubMed2000

A role for decorin in the structural organization of periodontal ligament.

Decorin is a small leucine-rich proteoglycan that interacts with several matrix molecules, including various types of collagen and growth factors, and suppresses the growth of neoplastic cells by an epidermal growth factor (EGF) receptor-mediated pathway. Decorin is abundantly expressed in the periodontal connective tissues during development and tissue maintenance. In periodontal disease, which is one of the most common diseases in the human kind, the level of decorin is decreased in the periodontal connective tissue. Abnormal expression of decorin may also associate with certain inherited disorders that involve increased susceptibility to severe periodontal disease in the early childhood. Therefore, we investigated the periodontal tissues of mice with targeted disruption of the decorin gene. Gross and microscopic analyses showed that decorin-deficient mice appeared to have normal tooth development and eruption, and there were no signs of periodontal disease. However, electron microscopic analysis revealed abnormal morphology and organization of the collagen fibrils in the periodontal ligament. The number of periodontal ligament fibroblasts in the decorin-deficient mice was also increased about two-fold as compared with the wild-type mice. In cell culture, ectopic overexpression of decorin in NIH 3T3 fibroblasts or decorin added exogenously to periodontal fibroblasts suppressed cell growth. However, blocking the EGF receptor tyrosine kinase activity did not prevent the decorin-elicited growth suppression in periodontal fibroblasts. Additionally, decorin did not induce a marked increase in the relative expression of p21 mRNA in periodontal fibroblasts. Therefore, decorin appeared to regulate growth of normal periodontal fibroblasts by a mechanism distinct from that reported for neoplastic cells. The findings demonstrate that decorin plays a role in the organization of collagen fibrils and regulates cell proliferation in the periodontal ligament.

3T3 Cells↗

PubMed2026

Machine learning-based analysis of oral rinse samples to identify candidate proteomic signatures for severe periodontitis: a pilot study.

This pilot study investigated whether candidate protein signatures from oral rinse samples can distinguish patients with severe periodontitis (stage III/IV) and its subtypes, generalized and localized periodontitis, from non-periodontitis controls. Participants rinsed with phosphate-buffered saline, and samples were analyzed using a Proximity Extension Assay targeting 92 inflammatory and 92 immuno-oncology proteins. A machine learning approach using repeated nested cross-validation and SHAP was implemented to identify protein signatures. The study included 38 patients (18 with localized periodontitis and 20 with generalized periodontitis) and 16 controls. After data preprocessing, 54 samples and 141 proteins were retained. Proteins Gal-1, HGF, TNFSF14, CD27, and ARG1 distinguished periodontitis from controls (ROC-AUC = 0.85, 95% CI 0.82, 0.87). For generalized periodontitis, we found a protein signature including TNFSF14, Gal-1, STAMBP, MUC-16, S100A12, HGF, CASP-8, CD27, LAP TGF-β1, TNFRSF9, and uPA (ROC-AUC = 0.92, 95% CI 0.90, 0.94). For localized periodontitis, we identified ARG1 (ROC-AUC = 0.72, 95% CI 0.68, 0.76). No proteomic signature distinguishing generalized periodontitis from localized periodontitis was identified. This pilot study indicated that oral rinses are suitable for proteomic profiling, and there was a putative protein signature that could differentiate periodontitis, generalized periodontitis, and localized periodontitis from controls. These findings warrant validation in larger independent cohorts, including a clearly defined gingivitis group, before real-world non-invasive screening applications can be considered.

Humans↗

PubMed2006

Salivary aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase: possible markers in periodontal diseases?

BACKGROUND: Saliva can be used as a diagnostic fluid in medicine. Components of saliva proposed as disease markers include enzymes (alkaline phosphatase, esterase, glucuronidase, aminopeptidase), immunoglobulins (IgA, IgG), and hormones (steroid hormones). Many of these salivary components appeared to be useful biochemical markers of the evolution of periodontal disease, for which salivary analysis can offer a cost-effective approach for monitoring the disease. The salivary components proposed as markers for periodontal disease activity are aspartate aminotransferase (AST), alkaline phosphatase (ALP), aminopeptidases, and glucuronidases. The purpose of our study was to illustrate the influence of periodontal disease on the level of salivary AST, alanine aminotransferase (ALT) and ALP. METHODS: All clinical periodontal examinations were performed by the same periodontist. All patients included in the study presented a probing depth >5 mm, bleeding on probing and alveolar bone loss >40%. Salivary AST, ALT and ALP activities were measured using DiaSys analysis kits from Diagnostic Systems. The methods were adapted for saliva. RESULTS: Salivary AST activity in patients with periodontal disease was significantly increased (p<0.01) (median 81.75+/-23 U/L) compared with controls (15.25+/-10.5 U/L). Salivary ALT activity was not significantly modified in saliva from patients with periodontal disease compared with the control group. Our results showed a significant (p<0.01) increase in salivary ALP activity (34.38+/-1.5 U/L) in patients with periodontal disease compared with controls (6.6+/-4.2 U/L). CONCLUSIONS: Our results revealed that periodontal destruction such as periodontal pockets, gingival bleeding and suppuration are related to higher ALP and AST levels in saliva. Salivary AST could be used as a useful marker for monitoring periodontal disease. The increase in salivary ALP activity in periodontitis demonstrated could be associated with alveolar bone loss, a key feature of periodontal disease. More studies are necessary to evaluate which specific clinical, microbiological and histological characteristics of periodontal disease are associated with elevated levels of AST and ALP in saliva.

Adult↗

PubMed1998

Epidemiological and clinical aspects of periodontal diseases in diabetics.

The association between diabetes mellitus and periodontal disease has long been discussed, with conflicting conclusions. On the one hand, numerous reports indicate a high prevalence of periodontal disease in diabetics compared to healthy controls, while others fail to show such a relationship. Clarification of this dilemma has been occurring as the diagnostic criteria for periodontal disease destruction improve and the number and size of the populations surveyed grow. This review is based on a selective review of the literature from the present decade. To date, based mainly on an extensive study of the Pima Indians who have an extremely high incidence of non-insulin-dependent diabetes mellitus (NIDDM), it seems to be clear that patients with NIDDM have a higher prevalence and severity of periodontal disease destruction than non-diabetics in the same population. However, it must be borne in mind that these data are for a special population. Studies on patients with insulin-dependent diabetes mellitus (IDDM) indicate results similar to those found in studies on NIDDM. There is an increase in prevalence and severity of periodontitis compared to controls. For both IDDM and NIDDM, there does not appear to be any correlation between the prevalence or the severity of periodontal disease and the duration of diabetes. Well-controlled diabetic patients as measured by blood glycated hemoglobin levels have less severe periodontal disease than poorly controlled diabetics. The principles of treatment of periodontitis in diabetics are the same as those for non-diabetic patients and are consistent with our approach to all high-risk patients who have already developed periodontal disease. The major efforts should be directed at the prevention of periodontitis in patients at risk of developing diabetes. Another important clinical question relates to the influence of periodontal disease on the control of the diabetic state. Here again the literature is unclear; however, a recent development suggests that effective control of periodontal infection in patients with diabetes reduces the level of advanced glycosylation end products in the serum. If future studies can confirm this effect, then periodontal infection control must be considered an integral part of diabetic control.

Diabetes Complications↗

PubMed2001

Periodontitis and diabetes interrelationships: role of inflammation.

Diabetes mellitus is a systemic disease with several major complications affecting both the quality and length of life. One of these complications is periodontal disease (periodontitis). Periodontitis is much more than a localized oral infection. Recent data indicate that periodontitis may cause changes in systemic physiology. The interrelationships between periodontitis and diabetes provide an example of systemic disease predisposing to oral infection, and once that infection is established, the oral infection exacerbates systemic disease. In this case, it may also be possible for the oral infection to predispose to systemic disease. In order to understand the cellular/molecular mechanisms responsible for such a cyclical association, one must identify common physiological changes associated with diabetes and periodontitis that produce a synergy when the conditions coexist. A potential mechanistic link involves the broad axis of inflammation, specifically immune cell phenotype, serum lipid levels, and tissue homeostasis. Diabetes-induced changes in immune cell function produce an inflammatory immune cell phenotype (upregulation of proinflammatory cytokines from monocytes/polymorphonuclear leukocytes and downregulation of growth factors from macrophages). This predisposes to chronic inflammation, progressive tissue breakdown, and diminished tissue repair capacity. Periodontal tissues frequently manifest these changes because they are constantly wounded by substances emanating from bacterial biofilms. Diabetic patients are prone to elevated low density lipoprotein cholesterol and triglycerides (LDL/TRG) even when blood glucose levels are well controlled. This is significant, as recent studies demonstrate that hyperlipidemia may be one of the factors associated with diabetes-induced immune cell alterations. Recent human studies have established a relationship between high serum lipid levels and periodontitis. Some evidence now suggests that periodontitis itself may lead to elevated LDL/TRG. Periodontitis-induced bacteremia/endotoxemia has been shown to cause elevations of serum proinflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), which have been demonstrated to produce alterations in lipid metabolism leading to hyperlipidemia. Within this context, periodontitis may contribute to elevated proinflammatory cytokines/serum lipids and potentially to systemic disease arising from chronic hyperlipidemia and/or increased inflammatory mediators. These cytokines can produce an insulin resistance syndrome similar to that observed in diabetes and initiate destruction of pancreatic beta cells leading to development of diabetes. Thus, there is potential for periodontitis to exacerbate diabetes-induced hyperlipidemia, immune cell alterations, and diminished tissue repair capacity. It may also be possible for chronic periodontitis to induce diabetes.

Bacteremia↗

PubMed2001

The relationship between periodontal diseases and diabetes: an overview.

Diabetes mellitus, caused by the malfunction of insulin-dependent glucose and lipid metabolism, presents with the classical triad of symptoms: polydypsia, polyuria, and polyphagia which are often accompanied by chronic fatigue and loss of weight. Complications of diabetes mellitus include retinopathy, nephropathy, neuropathy, and cardiovascular disease. Periodontal diseases are infections affecting the periodontium and resulting in the loss of tooth support. The association between diabetes mellitus and periodontitis has long been discussed with conflicting conclusions. Both of these diseases have a relatively high incidence in the general population (diabetes 1% to 6% and periodontitis 14%) as well as a number of common pathways in their pathogenesis (both diseases are polygenic disorders with some degree of immunoregulatory dysfunction). On the one hand, numerous reports indicate a higher incidence of periodontitis in diabetics compared to healthy controls, while other reports fail to show such a relationship. Clarification of this dilemma is occurring as the diagnostic criteria for periodontitis and diabetes mellitus improve, controlled studies with increased sample sizes are carried out, and the studies take into account major confounding variables that impact on the pathogenesis of both diseases. Current studies tend to support a higher incidence and severity of periodontitis in patients with diabetes mellitus. The overview looks at the bidirectional relationship between periodontitis and diabetes. An analysis of the National Health and Nutrition Examination Survey (NHANES) III data set confirms the previously reported significantly higher prevalence of periodontitis in diabetics than in non-diabetics (17.3% versus 9%). The analysis of the data also shows that the prevalence of diabetes in patients with periodontitis is double that seen in the non-periodontitis patients (12.5% versus 6.3%) and that this difference is also statistically significant. The pathogenesis of the 2 diseases is reviewed with an emphasis on common genetic and immune mechanisms. On the basis of the overview, 2 hypotheses for testing the relationship between periodontitis and diabetes are discussed. The first proposes a direct causal or modifying relationship in which the hyperglycemia and hyperlipidemia of diabetes result in metabolic alterations that may then exacerbate bacteria-induced inflammatory periodontitis. The second hypothesis proposes that a fortuitous combination of genes (gene sets) could result in a host who, under the influence of a variety of environmental stressors, could develop either periodontitis or diabetes or both.

Diabetes Complications↗

PubMed2003

Periodontal disease as a risk factor for adverse pregnancy outcomes. A systematic review.

BACKGROUND: Recent studies have implicated a variety of infections, including periodontal diseases, as risk factors for adverse pregnancy outcomes such as prematurity and low birth weight. RATIONALE: A number of studies have shown that bacterial vaginosis is related to preterm and/or low birth weight (PT/LBW), which continues to be a significant cause of infant morbidity and mortality. It is also possible that other infectious processes, including periodontal diseases, contribute to PT/LBW. This systematic review examines the literature to determine the possible relationship between PT/LBW and periodontal diseases. FOCUSED QUESTION: Does prevention/control of periodontal disease as compared to controls have an impact on the initiation/progression of adverse pregnancy outcomes? SEARCH PROTOCOL: MEDLINE, pre-MEDLINE, MEDLINE Daily Update, and the Cochrane Oral Controlled Trials Register were searched to identify published studies that related variables associated with PT/LBW and periodontal disease. Searches were performed for articles published through October 2002. INCLUSION CRITERIA: Randomized controlled clinical trials (RCTs), case-control, and cohort studies were included. Study populations included mothers, with or without periodontal disease, who gave birth to preterm and/or mature infants. The interventions considered included all forms of periodontal therapy. EXCLUSION CRITERIA: Only studies on humans were included. DATA COLLECTION AND ANALYSIS: Due to study heterogeneity, meta-analysis was not possible. MAIN RESULTS: 1. Of the over 660 studies identified, 12 (6 case-control, 3 cross-sectional and longitudinal, and 3 intervention) met inclusion and exclusion criteria and were included in the analysis. 2. While several studies implicated periodontal disease as a risk factor for PT/LBW, few assessed the impact of the prevention and treatment of periodontal disease on outcomes. 3. Several epidemiologic studies did not support periodontal disease as a risk factor for PT/LBW. REVIEWERS' CONCLUSIONS: 1. Periodontal disease may be a risk factor for PT/LBW. 2. Additional longitudinal, epidemiologic, and interventional studies are needed to validate this association and to determine whether it is causal. 3. It is not yet clear whether periodontal diseases play a causal role in adverse pregnancy outcomes. 4. Preliminary evidence to date suggests that periodontal intervention may reduce adverse pregnancy outcomes.

Consensus↗