Advanced Lemierre syndrome requiring surgery

A 38-year-old homeless man was admitted with a 2-week history of a sore throat, increasing shortness of breath, and high fever. Clinical examination showed enlarged and tender submandibular and anterior cervical lymph nodes and a pronounced enlargement of the left peritonsillar region (Figure 1a). CT scan of the throat and the chest showed left peritonsillar abscess formation, occlusion of the left internal jugular vein with inflammatory wall thickening and perijugular soft tissue infiltration, pulmonary abscesses, and bilateral pleural effusions (Figures 1b-e, arrowed). Anaerobe blood cultures grew Fusobacterium necrophorum, leading to the diagnosis of Lemierre's syndrome. Treatment with high-dose amoxicillin and clavulanic acid improved the oropharyngeal condition, but the patient's general status declined further, marked by dyspnea and tachypnea. Repeated CT scans showed progressive lung abscesses and bilateral pleural empyema. Bilateral tonsillectomy, ligation of the left internal jugular vein, and staged decortication of bilateral empyema were performed. Total antibiotic therapy duration was 9 weeks, including a change to peroral clindamycin. Clinical and laboratory findings had returned to normal 12 weeks after surgery.The patient's history and the clinical and radiological findings are characteristic for Lemierre's syndrome. CT scans of the neck and the chest are the diagnostic methods of choice. F. necrophorum is found in over 80% of cases of Lemierre's syndrome and confirms the diagnosis. Prolonged antibiotic therapy is usually sufficient, but in selected patients, a surgical intervention may be necessary. Reported mortality rates are high, but in surviving patients, the recovery of pulmonary function is usually good.

Microbiota at teeth and implants in partially edentulous patients. A 10-year retrospective study.

OBJECTIVE To determine the microbiota at implants and adjacent teeth 10 years after placement of implants with a sandblasted and acid-etched surface. MATERIAL AND METHODS Plaque samples obtained from the deepest sites of 504 implants and of 493 adjacent teeth were analyzed for certain bacterial species associated with periodontitis, for staphylococci, for aerobic gram-negative rods, and for yeasts using nucleic acid-based methods. RESULTS Species known to be associated with periodontitis were detectable at 6.2-78.4% of the implants. Significantly higher counts at implants in comparison with teeth were assessed for Tannerella forsythia, Parvimonas micra, Fusobacterium nucleatum/necrophorum, and Campylobacter rectus. Higher counts of periodontopathogenic species were detectable at implants of current smokers than at those of non-smokers. In addition, those species were found in higher quantities at implants of subjects with periodontitis. The prevalence of Prevotella intermedia, Treponema denticola, C. rectus, and moreover of Staphylococcus warneri might be associated with peri-implant inflammation. Selected staphylococcal species (not Staphylococcus aureus), aerobic gram-negative rods, and yeasts were frequently detected, but with the exception of S. warneri, they did not show any association with periodontal or peri-implant diseases. CONCLUSIONS Smoking and periodontal disease are risk factors for colonization of periodontopathic bacteria at implants. Those bacterial species may play a potential role in peri-implant inflammation. The role of S. warneri needs further validation.

Mixture of periodontopathogenic bacteria influences interaction with KB cells

INTRODUCTION: The purpose of this study was to investigate the adhesion and invasion of periodontopathogenic bacteria in varied mixed infections and the release of interleukins from an epithelial cell line (KB cells). METHODS: KB cells were co-cultured with Porphyromonas gingivalis ATCC 33277 and M5-1-2, Tannerella forsythia ATCC 43037, Treponema denticola ATCC 35405 and Fusobacterium nucleatum ATCC 25586 in single and mixed infections. The numbers of adherent and internalized bacteria were determined up to 18 h after bacterial exposure. Additionally, the mRNA expression and concentrations of released interleukin (IL)-6 and IL-8 were measured. RESULTS: All periodontopathogenic bacteria adhered and internalized in different numbers to KB cells, but individually without any evidence of co-aggregation also to F. nucleatum. High levels of epithelial mRNA of IL-6 and IL-8 were detectable after all bacterial challenges. After the mixed infection of P. gingivalis ATCC 33277 and F. nucleatum ATCC 25586 the highest levels of released interleukins were found. No IL-6 and IL-8 were detectable after the mixed infection of P. gingivalis M5-1-2 and F. nucleatum ATCC 25586 and the fourfold infection of P. gingivalis ATCC 33277, T. denticola ATCC 35405, T. forsythia ATCC 43037 and F. nucleatum ATCC 25586. CONCLUSION: Anaerobic periodontopathogenic bacteria promote the release of IL-6 and IL-8 by epithelial cells. Despite a continuous epithelial expression of IL-8 mRNA by all bacterial infections these effects are temporary because of the time-dependent degradation of cytokines by bacterial proteases. Mixed infections have a stronger virulence potential than single bacteria. Further research is necessary to evaluate the role of mixed infections and biofilms in the pathogenesis of periodontitis.

Mechanical non-surgical treatment of peri-implantitis: a single-blinded randomized longitudinal clinical study. II. Microbiological results

BACKGROUND: Peri-implantitis is common in patients with dental implants. We performed a single-blinded longitudinal randomized study to assess the effects of mechanical debridement on the peri-implant microbiota in peri-implantitis lesions. MATERIALS AND METHODS: An expanded checkerboard DNA-DNA hybridization assay encompassing 79 different microorganisms was used to study bacterial counts before and during 6 months following mechanical treatment of peri-implantitis in 17 cases treated with curettes and 14 cases treated with an ultrasonic device. Statistics included non-parametric tests and GLM multivariate analysis with p<0001 indicating significance and 80% power. RESULTS: At selected implant test sites, the most prevalent bacteria were: Fusobacterium nucleatum sp., Staphylococci sp., Aggregatibacter actinomycetemcomitans, Helicobacter pylori, and Tannerella forsythia. 30 min. after treatment with curettes, A. actinomycetemcomitans (serotype a), Lactobacillus acidophilus, Streptococcus anginosus, and Veillonella parvula were found at lower counts (p<0.001). No such differences were found for implants treated with the ultrasonic device. Inconsistent changes occurred following the first week. No microbiological differences between baseline and 6-month samples were found for any species or between treatment study methods in peri-implantitis. CONCLUSIONS: Both methods failed to eliminate or reduce bacterial counts in peri-implantitis. No group differences were found in the ability to reduce the microbiota in peri-implantitis.

Effect of ozone on periodontopathogenic species--an in vitro study

The in vitro study was aimed to determine the effect of ozone on periodontopathogenic microorganisms. Ozone was generated for 6 s-2 × 24 s (corresponding to 0.56 mg-2 × 2.24 mg of ozone) against 23 mainly anaerobic periodontopathogenic species. Agar diffusion test was used as a screening method. Then, the killing activity was tested in a serum-free environment and with 25% v/v inactivated serum. Further, the effect of ozone on bactericidal activity of native serum was analyzed against Fusobacterium nucleatum, Porphyromonas gingivalis, and Aggregatibacter actinomycetemcomitans. Agar diffusion test showed a high efficacy of ozone against microorganisms, especially against Porphyromonas gingivalis. This result was confirmed by the killing tests; most of the strains in a concentration of 10(5) were completely eliminated after twofold 18-s application of ozone. Only four of the six potentially "superinfecting" species (Staphylococcus aureus, Enterococcus faecalis, Enterobacter cloacae, Candida albicans) survived in part. Addition of heat-inactivated serum reduced the killing rate of ozone by 78% after 6-s and by 47% after twofold 18-s exposures; no strain was completely eradicated after any application of ozone. The bactericidal effect of native serum was enhanced after application of ozone; no effect was visible on the included A. actinomycetemcomitans strain which was found to be completely resistant to the bactericidal action of serum. In conclusion, (a) ozone has a strong antibacterial activity against putative periodontopathogenic microorganisms, and (b) the bactericidal effect is reduced in the presence of serum. Ozone may have potential as an adjunctive application to mechanical treatment in periodontitis patients.

Comparison of bacterial plaque samples from titanium implant and tooth surfaces by different methods

Studies have shown similarities in the microflora between titanium implants or tooth sites when samples are taken by gingival crevicular fluid (GCF) sampling methods. The purpose of the present study was to study the microflora from curette and GCF samples using the checkerboard DNA-DNA hybridization method to assess the microflora of patients who had at least one oral osseo-integrated implant and who were otherwise dentate. Plaque samples were taken from tooth/implant surfaces and from sulcular gingival surfaces with curettes, and from gingival fluid using filter papers. A total of 28 subjects (11 females) were enrolled in the study. The mean age of the subjects was 64.1 years (SD+/-4.7). On average, the implants studied had been in function for 3.7 years (SD+/-2.9). The proportion of Streptococcus oralis (P<0.02) and Fusobacterium periodonticum (P<0.02) was significantly higher at tooth sites (curette samples). The GCF samples yielded higher proportions for 28/40 species studies (P-values varying between 0.05 and 0.001). The proportions of Tannerella forsythia (T. forsythensis), and Treponema denticola were both higher in GCF samples (P<0.02 and P<0.05, respectively) than in curette samples (implant sites). The microbial composition in gingival fluid from samples taken at implant sites differed partly from that of curette samples taken from implant surfaces or from sulcular soft tissues, providing higher counts for most bacteria studied at implant surfaces, but with the exception of Porphyromonas gingivalis. A combination of GCF and curette sampling methods might be the most representative sample method.

The Subgingival Microbiota in older subjects. Impact of Chlorhexidine Rinsing

Background: Periodontitis and caries are common diseases in older adults. Aims: To test if rinsing with chlorhexidine over five years has an impact on the subgingival microbiota. Methods: In a double blind randomized five years chlorhexidine rinse study clinical oral data and subgingival plaque samples were analyzed by the checkerboard DNA-DNA hybridization method. Results: At year 5 subject mean age was 71.2 years (S.D. + 4.1) (56.2% women). Only in subjects with no bone loss did the chlorhexidine rinse group subjects presented with lower total bacterial (DNA) counts (mean diff: 63.1 (x105), S.E diff + 30.1 (x105), 95%CI: 0.8 to 120.5 (x105), p<0.05) [(i.e.Lactobacillus acidophilicus (p<0.05) , Streptococcus oralis (p<0.05), Eikenella. corrodens (p< 0.05), C. gracilis (p<0.01), F.nucl.sp. nucleatum (p< 0.02), Fusobacterium nucl. sp. polymorphum (p<0.02), Neisseria mucosa (p<0.02), Leptothrichia buccalis (p<0.02), and Selenomonas noxia (p<0.050)]. Higher bacterial loads were found for the green (p<0.05), yellow (streptococci spp) (p<0.01), and the ‘other' complexes (p<0.01). Conclusions: Independent of probing pocket depth, older subjects carry a large variety of bacteria associated with periodontitis. The oral microbiota in older subjects is linked to alveolar bone loss and not to probing depth. Chlorhexidine may provide a benefit in preventing periodontitis in older persons.

Infection at titanium implants with or without clinical inflammation

Objectives: The aims of the present study were (1)to assess the microbiota at implants in function diagnosed as having either peri-implantitis, or mucositis, or being clinically without symptoms of inflammation, (2) to identify explanatory factors to implant status. Material and Methods: Clinical and microbiological data were collected from 138 subjects (mean age: 62.3 ± 14.9) with 524 implants in function for an average of 10.8 years (S.D. +1.5). The checkerboard DNA-DNA hybridization method was used to identify 40 bacterial species. Results: Subjects had poor oral hygiene with a mean % plaque score 53.2 ± 24.4. In 36% of cases periodontitis was reported as the cause for implant therapy. Mucositis was diagnosed in 61.6% and per-implantitis in 15.9% of all cases. Edentulous subjects had at implants with peri-implantitis significantly higher bacterial loads for Streptococcus sanguis (p<0.01), Fusobacterium nucleatum sp. nucleatum (p<0.02), and Leptothrichia buccalis (p<0.05) than did dentate implant subjects. Dentate subjects had higher bacterial loads of Porphyromonas gingivalis (p<0.02). The levels of Fusobacterium nucleatum sp.vincentii and Capnocytophaga ochracea were explanatory to mucositis. Only a history of periodontitis as cause of tooth loss and smoking were explanatory to peri-implantitis. The microbiota was not affect by supportive care patterns. Conclusions: Presence or absence of teeth partly explains the implant microbiota. A past history of periodontitis and smoking are associated with peri-implantitis. The microbiota at implants with mucositis, or peri-implantitis is similar to that of teeth. Supportive periodontal and implant therapy fails to have an impact on implant microbiota and does not prevent mucositis and peri-implantitis.

The impact of a low-frequency chlorhexidine rinsing schedule on the subgingival microbiota (the TEETH clinical trial)

BACKGROUND: Information on the efficacy of chlorhexidine (CHX) rinsing on the subgingival microbiota is limited. This study tested if intermittent CHX rinsing over 5 years had an impact on the subgingival microbiota. METHODS: Subgingival plaque samples were analyzed by the checkerboard DNA-DNA hybridization method in a double-blind randomized CHX rinse study. RESULTS: A total of 210 subjects were included. The mean age of the subjects was 71.7 (+/- 4.1) years, and 56.2% were women. Evidence of alveolar bone loss was found in 39% of subjects. Bacterial loads were not correlated significantly with probing depth. At year 5, subjects in the CHX rinse group with no evidence of bone loss presented with lower total bacterial counts than control subjects with no bone loss. The levels of the following bacteria were significantly lower in the CHX group: Lactobacillus acidophilus (P <0.05), Eikenella corrodens (P <0.05), Fusobacterium nucleatum sp. nucleatum (P <0.01), Treponema denticola (P <0.05), Leptotrichia buccalis (P <0.05), and Eubacterium saburreum (P <0.05). No differences in bacterial loads were found between CHX and control rinse subjects with alveolar bone loss. CONCLUSIONS: Older subjects with or without periodontitis carry a large variety of bacteria associated with periodontitis. Intermittent rinsing with CHX may provide a preventive benefit in reducing levels of bacteria but only in subjects without alveolar bone loss.

Infection at titanium implants with or without a clinical diagnosis of inflammation

OBJECTIVES: To assess the microbiota at implants diagnosed with peri-implantitis, implant mucositis, or being clinically healthy. MATERIAL AND METHODS: Clinical and microbiological data were collected from 213 subjects (mean age: 65.7+/-14) with 976 implants in function (mean: 10.8 years, SD+/-1.5). Forty species were identified by the checkerboard DNA-DNA hybridization method. RESULTS: Implant mean % plaque score was 41.8+/-32.4%. Periodontitis defined by bone loss was found in 44.9% of subjects. Implant mucositis was diagnosed in 59% and peri-implantitis in 14.9% of all cases. Neisseria mucosa, Fusobacterium nucleatum sp. nucleatum, F. nucleatum sp. polymorphum, and Capnocytophaga sputigena dominated the implant sub-mucosal microbiota and the sub-gingival microbiota at tooth sites. Implant probing pocket depth at the implant site with the deepest probing depth was correlated with levels of Eikenella corrodens (r=0.16, P<0.05), the levels of F. nucleatum sp. vincentii (r=0.15, P<0.05), Porphyromonas gingivalis (r=0.14, P<0.05), and Micromonas micros (r=0.17, P=0.01). E. corrodens was found in higher levels at implants with mucositis compared with implant health (P<0.05). Subjects who lost teeth due to periodontitis had higher yields of F. nucleatum sp. vincentii (P<0.02) and N. mucosa (P<0.05). Independent of implant status subjects with teeth had higher levels of P. gingivalis (P<0.05), and Leptotrichia buccalis (P<0.05). CONCLUSIONS: At implant sites studied, few bacteria differed by whether subjects were dentate or not or by implant status.

Two-year outcome with Nobel Direct implants: a retrospective radiographic and microbiologic study in 10 patients

INTRODUCTION: The Nobel Direct implant (Nobel Biocare AB, Göteborg, Sweden) was developed to minimize marginal bone resorption and to result in "soft tissue integration" for an optimized aesthetic outcome. However, conflicting results have been presented in the literature. The aim of this present study was to evaluate the clinical and microbiologic outcomes of Nobel Direct implants. MATERIALS AND METHODS: Ten partially edentulous subjects without evidence of active periodontitis (mean age 55 years) received 12 Nobel Direct implants. Implants were loaded with single crowns after a healing period of 3 to 6 months. Treatment outcomes were assessed at month 24. Routine clinical assessments, intraoral radiographs, and microbiologic samplings were made. Histologic analysis of one failing implant and chemical spectroscopy around three unused implants was performed. Paired Wilcoxon signed-rank test was used for the evaluation of bone loss; otherwise, descriptive analysis was performed. RESULTS: Implants were functionally loaded after 3 to 6 months. At 2 years, the mean bone loss of remaining implants was 2.0 mm (SD +/- 1.1 mm; range: 0.0-3.4 mm). Three out of 12 implants with an early mean bone loss >3 mm were lost. The surviving implants showed increasing bone loss between 6 and 24 months (p = .028). Only 3 out of the 12 implants were considered successful and showed bone loss of <1.7 mm after 2 years. High rates of pathogens, including Aggregatibacter actinomycetemcomitans, Fusobacterium spp., Porphyromonas gingivalis, Pseudomonas aeruginosa, and Tanerella forsythia, were found. Chemical spectroscopy revealed, despite the normal signals from Ti, O, and C, also peaks of P, F, S, N, and Ca. A normal histologic image of osseointegration was observed in the apical part of the retrieved implant. CONCLUSION: Radiographic evidence and 25% implant failures are indications of a low success rate. High counts and prevalence of significant pathogens were found at surviving implants. Although extensive bone loss had occurred in the coronal part, the apical portion of the implant showed some bone to implant integration.

[Periodontitis and cardiovascular disease]

The prevalence of periodontitis and cardiovascular disease (CVD) is high. A mixed infectious biofilm etiology of periodontitis is known but not fully established in CVD. Cofactors; smoking habits, stress, ethnicity, genetics, socioeconomics and age contribute to both diseases. The objectives of this report are to summarize factors in regards to CVD and periodontitis that are clinically relevant. The hypothesis behind a relationship between the two conditions can be founded in (I) shared infections etiology, (II) shared inflammatory response, (III) epidemiological and case-control studies, and (IV) periodontal studies demonstrating improvements of CVD markers. Streptococcus species in the S. mitis group, and S. anginosus group have been identified in periodontitis and are known as pathogens in endocarditis possibly transported from the oral cavity to the heart through bacteremia during dental therapies, and tooth brushing. Other periodontal bacteria such as Porphyromonas gingivalis, Fusobacterium nucleatum and Parvimonas micra are beta-lactamase producing and may contribute to antibiotic resistance (extended spectrum beta-lactamases). Other bacteria in CVD and periodontitis include Staphylococcus aureus, and Pseudomonas aeruginosa. Chlamydia pneumoniae and P. gingivalis lipopolyysaccharide capsels share homology and induce heat-shock protein activity and a cascade of proinflammatory cytokines. Associations between periodontitis and CVD have been presented in many studies when controlling for confounders. Other studies have demonstrated that periodontal therapies increase brachial artery flow rate and reduce serum inflammatory cytokine levels. Thus, physicians caring for subjects at CVD risk should consult with dentists/periodontists. Dentists must improve their medical knowledge and also learn to consult with physicians when treating patients at CVD risk.

Does pregnancy have an impact on the subgingival microbiota?

BACKGROUND: We investigated clinical and subgingival microbiologic changes during pregnancy in 20 consecutive pregnant women > or =18 years not receiving dental care. METHODS: Bacterial samples from weeks 12, 28, and 36 of pregnancy and at 4 to 6 weeks postpartum were processed for 37 species by checkerboard DNA-DNA hybridization. Clinical periodontal data were collected at week 12 and at 4 to 6 weeks postpartum, and bleeding on probing (BOP) was recorded at sites sampled at the four time points. RESULTS: The mean BOP at week 12 and postpartum was 40.1% +/- 18.2% and 27.4% +/- 12.5%, respectively. The corresponding mean BOP at microbiologic test sites was 15% (week 12) and 21% (postpartum; not statistically significant). Total bacterial counts decreased between week 12 and postpartum (P <0.01). Increased bacterial counts over time were found for Neisseria mucosa (P <0.001). Lower counts (P <0.001) were found for Capnocytophaga ochracea, Capnocytophaga sputigena, Eubacterium saburreum, Fusobacterium nucleatum naviforme, Fusobacterium nucleatum polymorphum, Leptotrichia buccalis, Parvimonas micra (previously Peptostreptococcus micros or Micromonas micros), Prevotella intermedia, Prevotella melaninogenica, Staphylococcus aureus, Streptococcus anginosus, Streptococcus intermedius, Streptococcus mutans, Streptococcus oralis, Streptococcus sanguinis, Selenomonas noxia, and Veillonella parvula. No changes occurred between weeks 12 and 28 of pregnancy. Counts of Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Porphyromonas gingivalis, Tannerella forsythia (previously T. forsythensis), and Treponema denticola did not change. Counts of P. gingivalis and T. forsythia at week 12 were associated with gingivitis (P <0.001). CONCLUSIONS: Subgingival levels of bacteria associated with periodontitis did not change. P. gingivalis and T. forsythia counts were associated with BOP at week 12. A decrease was found in 17 of 37 species from week 12 to postpartum. Only counts of N. mucosa increased.

The impact of the stone age diet on gingival conditions in the absence of oral hygiene

BACKGROUND: The objective of this study was to assess the oral microbiota and clinical data in subjects without access to traditional oral hygiene methods and who ate a diet available in the Stone Age. METHODS: Ten subjects living in an environment replicating the Stone Age for 4 weeks were enrolled in this study. Bleeding on probing (BOP), gingival and plaque indices, and probing depth (PD) were assessed at baseline and at 4 weeks. Microbiologic samples were collected at the mesio-buccal subgingival aspects of all teeth and from the dorsum of the tongue and were processed by checkerboard DNA-DNA hybridization methods. RESULTS: No subject had periodontitis. Mean BOP decreased from 34.8% to 12.6% (P <0.001). Mean gingival index scores changed from 0.38 to 0.43 (not statistically significant) and mean plaque scores increased from 0.68 to 1.47 (P <0.001). PD at sites of subgingival sampling decreased (mean difference: 0.2 mm; P <0.001). At week 4, the total bacterial count was higher (P <0.001) for 24 of 74 species, including Bacteroides ureolyticus, Eikenella corrodens, Lactobacillus acidophilus, Capnocytophaga ochracea, Escherichia coli, Fusobacterium nucleatum naviforme, Haemophilus influenzae, Helicobacter pylori, Porphyromonas endodontalis, Staphylococcus aureus (two strains), Streptococcus agalactiae, Streptococcus anginosis, and Streptococcus mitis. Bacterial counts from tongue samples were higher at baseline (P <0.001) for 20 species, including Tannerella forsythia (previously T. forsythensis), Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans; serotype a), and Streptococcus spp. CONCLUSIONS: The experimental gingivitis protocol is not applicable if the diet (e.g., Stone Age) does not include refined sugars. Although plaque levels increased, BOP and PD decreased. Subgingival bacterial counts increased for several species not linked to periodontitis, whereas tongue bacterial samples decreased during the study period.

Regulation of visfatin by microbial and biomechanical signals in PDL cells

OBJECTIVES This in vitro study was established to examine whether visfatin thought to be a link between periodontitis and obesity is produced by periodontal ligament (PDL) cells and, if so, whether its synthesis is modulated by microbial and/or biomechanical signals. MATERIALS AND METHODS PDL cells seeded on BioFlex® plates were exposed to the oral pathogen Fusobacterium nucleatum ATCC 25586 and/or subjected to biomechanical strain for up to 3 days. Gene expression of visfatin and toll-like receptors (TLR) 2 and 4 was analyzed by RT-PCR, visfatin protein synthesis by ELISA and immunocytochemistry, and NFκB nuclear translocation by immunofluorescence. RESULTS F. nucleatum upregulated the visfatin expression in a dose- and time-dependent fashion. Preincubation with neutralizing antibodies against TLR2 and TLR4 caused a significant inhibition of the F. nucleatum-upregulated visfatin expression at 1 day. F. nucleatum stimulated the NFκB nuclear translocation. Biomechanical loading reduced the stimulatory effects of F. nucleatum on visfatin expression at 1 and 3 days and also abrogated the F. nucleatum-induced NFκB nuclear translocation at 60 min. Biomechanical loading inhibited significantly the expression of TLR2 and TLR4 at 3 days. The regulatory effects of F. nucleatum and/or biomechanical loading on visfatin expression were also observed at protein level. CONCLUSIONS PDL cells produce visfatin, and this production is enhanced by F. nucleatum. Biomechanical loading seems to be protective against the effects of F. nucleatum on visfatin expression. CLINICAL RELEVANCE Visfatin produced by periodontal tissues could play a major role in the pathogenesis of periodontitis and the interactions with obesity and other systemic diseases.