OBJECTIVE: This study aimed to determine the possible relationship between periodontal disease and ankylosing spondylitis (AS) by evaluating clinical periodontal measurements and gingival crevicular fluid (GCF) levels of sclerostin, interleukin-1β (IL-1ß), and matrix metalloproteinase-8 (MMP-8) levels.
METHODS: Twenty-eight patients with AS (AS group) and 28 systemically healthy controls (C group) were enrolled in this study. Full-mouth periodontal measurements: plaque index, bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment level (CAL) measurements were obtained from all patients. AS-related parameters were included in the data analyses. An enzyme-linked immunosorbent assay determined GCF IL-1β, MMP-8, and sclerostin levels.
RESULTS: There were no significant differences in the clinical periodontal measurements between the two groups (p > 0.05). Interestingly, patients with AS had significantly lower GCF sclerostin levels than the C group (p < 0.05). But there were no statistical differences in the GCF levels of IL-1ß and MMP-8 between the two groups (p > 0.05). Serum C-reactive protein (CRP) levels strongly correlated with both BOP (r = 0.497, p < 0.05) and PPD (r = 0.570, p < 0.05) in the AS group. Bath AS Metrology Index (BASMI) also positively correlated with both BOP (r = 0.530, p < 0.05) and CAL (r = 0.568, p < 0.05). Similarly, Maastrıcht Ankylosing Spondylitis Enthesis Score (MASES) strongly correlated with both BOP (r = 0.487, p < 0.05) and CAL (r = 0.522, p < 0.05).
CONCLUSIONS: These results suggest that the patient\'s systemic condition may influence local sclerostin levels in GCF, and the strong correlations between periodontal measurements and AS-related parameters may indicate an interrelationship between inflammatory periodontal disease and AS.
CONCLUSIONS: The present study provides important information concerning the relationship between periodontal disease and ankylosing spondylitis.
BACKGROUND: Thai Clinical Trials.gov (TCTR20200908001) (08. September 2020).

Chronic periodontitis (CP) is the common form of inflammatory oral disease. Matrix metalloproteinases (MMPs) play a pivotal role in the progression of CP by degrading gingival tissue and its remodelling. Here, we conducted a case-control study to investigate a possible association of single-nucleotide polymorphism of MMP genes and their interaction with CP in the Indian population. A total of 357 DNA samples of venous blood was isolated, of which 157 were identified as CP patients and 200 were healthy individuals. Genotyping of six MMP genes (MMP1, MMP3, MMP7, MMP8, MMP12 and MMP13) was done using polymerase chain reaction following Sanger\'s method of sequencing. Statistical analyses were performed by SPSS v16.0, R package (SNPassoc). Gene-gene interactions were evaluated by MDR 3.0.2. The frequency of 6A allele of MMP3 -11715A-6A gene polymorphisms (36%) and G allele of MMP8 +17G-C gene polymorphisms (34%) were higher in the CP population compared with the healthy population (19% and 24%, respectively). A significant association of T allele of MMP8 -799C-T gene promoter polymorphism was found with CP (OR = 2.95, 95%CI = 2.16 - 4.04, P < 0.0001). Genotypic frequency of MMP12 -82A-G polymorphism is associated with CP risk while its allelic distribution is not (OR = 1.32, 95%CI = 0.93 - 1.88, P = 0.129). Gene-gene interactions show the best cross validation consistency model, i.e. MMP1 -519A-G X MMP7 -181A-G X MMP8 -799C-T polymorphismswith a value of 9/10. This gene-gene interaction shows that the significant association of MMP8 -799C-T polymorphism with CP increased susceptibility. Allelic distribution of MMP8+17G-C and MMP3-11715A-6A polymorphisms revealed their protective role towards decreased risk of CP. MMP1 -519A-G and MMP7 -181A-G polymorphisms show combinatorial synergistic effect on CP risk.

BACKGROUND: Dental implants consist in the treatment of choice to replace tooth loss. The knowledge that implant loss tends to cluster in subsets of individuals may indicate that host response is influenced by genetic factors. Matrix metalloproteinases (MMPs) are enzymes that contribute to degradation and removal of collagen from extracellular matrix.
OBJECTIVE: This case-control study aimed to investigate the haplotypic combination of MMP polymorphism (rs1144393, rs1799750, rs3025058, and rs11225395) and implant loss.
METHODS: Two hundred nonsmokers subjects were matched by gender, age, implant number and position and divided in control group, 100 patients with one or more healthy implants, and test group, and 100 patients with one or more implant failures. Genomic DNA was extracted from saliva and genotypes were obtained by PCR-RFLP.
RESULTS: A significant association of rs1799750 (MMP-1) and rs11225395 (MMP-8) polymorphism on early implant loss was demonstrated (P ≤ 0.001). Global haplotype analysis indicated a significant difference between both groups (P < 0.0001). Haplotype T-A-GG-5A-C had a statistically significant risk effect, while haplotype C-A-G-6A-C andT-G-2G-5A-C had a protective effect in implant loss.
CONCLUSIONS: The results of this study showed that MMPs haplotype are a risk factor to early implant loss.

Untreated periodontal disease may influence general health. However, how may a physician, who is not trained in periodontal probing, detect untreated periodontitis? Activated matrix metalloproteinase-8 (aMMP-8) in saliva correlates with periodontal probing parameters. Thus, sensitivity and specificity of a chair-side test for aMMP-8 to detect periodontitis were evaluated. Thirty cases [untreated chronic periodontitis (ChP); 15 generalized moderate and 15 generalized severe] and 30 controls [probing depths (PD) ≤3 mm, vertical probing attachment level (PAL-V) ≤2 mm at <30 % of sites) were examined periodontally (PD, PAL-V, bleeding on probing). Subsequently, the aMMP-8 test was performed. The test kit becomes positive with ≥25 ng/ml aMMP-8 in the sample. The aMMP-8 test was positive in 87 % of ChP and in 40 % of controls. That corresponds to a sensitivity of 87 % and a specificity of 60 %. The sensitivity to detect generalized severe ChP was 93 % (60 % specificity). Backward stepwise logistic regression analysis to explain positive aMMP-8 tests identified exclusively ChP with an odds ratio of 9.8 (p < 0.001). Positive results of the aMMP-8 test significantly correlate with generalized ChP. The aMMP-8 test may be used by physicians to detect periodontitis in their patients.

OBJECTIVE: Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are dysregulated in metabolic syndrome (MetS) and associated with atherosclerosis and cardiovascular disease (CVD). Previous studies on the association between MMPs/TIMPs and MetS are controversial. We aimed to evaluate circulating MMP-8, MMP-9 and TIMP-1 in a group of MetS individuals and healthy controls to find the potential marker associated with MetS and its components.
METHODS: 243 MetS individuals participated in a nested case-control design, of whom 63 were excluded (study subjects for analysis n=180; 87 MetS cases, 93 controls). We employed the International Diabetes Federation criteria using national waist circumference cutoffs for case definition. Anthropometric and biochemical measurements were done using standard methods.
RESULTS: Plasma MMP-8, TIMP-1, tumor necrosis factor-alpha (TNF-α), highly sensitive C-reactive protein (hs-CRP) and MMP-8/TIMP-1 ratio were significantly higher in MetS cases (P for all < 0.05). Each component of MetS except raised fasting plasma glucose positively correlated with MMP-8 and numbers of MetS components increased with higher MMP-8. In all regression models, MMP-8 was a significant predictor of MetS and in the final model the relationship persisted even after adjusting for pro-inflammatory cytokines hs-CRP and TNF-α (odds ratio=6.008, 95% confidence interval: 1.612-22.389, P=0.008).
CONCLUSIONS: Strong associations of MMP-8 with components of MetS in univariate, bivariate and multivariate models suggest plasma MMP-8 as a potential cardiometabolic risk marker for MetS. Higher MMP-8 in MetS is possibly mediated through mechanisms both dependent and independent of chronic low grade inflammation.

OBJECTIVE: Despite increasing evidence for an association of obstructive sleep apnea syndrome (OSAS) and periodontal disease, the pathophysiological linking mechanisms remain unclear. This study aims to evaluate the salivary and serum matrix metalloproteinase-2, -8, -9 (MMP-2, -8, -9), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), myeloperoxidase (MPO), neutrophil elastase (NE), neutrophil gelatinase-associated lipocalin (NGAL), as well as degree of activation of MMP-2, -9 of patients with and without OSAS.
METHODS: A total of 50 individuals were included in the study. There were 13, 17 and 20 individuals, respectively in the control (non-OSAS) group, mild-to-moderate OSAS and severe OSAS groups. Saliva, serum samples and clinical periodontal parameters were collected. Biofluid samples were analysed by immunofluorometric assay (IFMA), enzyme-linked immunosorbent assay (ELISA), western immunoblotting and gelatine zymography. Statistical analyses were performed using D\'Agostino-Pearson omnibus normality test, Kruskal-Wallis test and Spearman rho rank correlation analysis.
RESULTS: There were no statistically significant differences in clinical periodontal parameters between the study groups. Salivary NE and proMMP-2 levels were significantly lower in the OSAS groups than the control group (p<0.05). Serum proMMP-9 concentration and the degree of MMP-9 activation in saliva were significantly lower in the severe OSAS group than the control group (p<0.05). There were significant correlations between salivary and serum proMMP-9 and -2 concentrations (p<0.05). Serum proMMP-2, NE and salivary proMMP-9 and -2 negatively correlated with indicators of OSAS severity (p<0.05).
CONCLUSIONS: The present findings do not support a pathophysiological link between the severity of OSAS and clinical periodontal status via neutrophil enzymes or MMPs.

Periodontitis is a common infectious disease associated with increased risk for ischemic stroke though presently unclear mechanisms. In a case-control study, we investigated salivary levels of four periodontal pathogens, as well as systemic and local inflammatory markers. The population comprised 98 patients with acute ischemic stroke (mean ± SD, 68.2 ± 9.7 yrs; 45.9% women) and 100 healthy controls (69.1 ± 5.2 yrs; 47.0% women). Patients were more often edentulous and had fewer teeth than controls (13.8 ± 10.8 versus 16.6 ± 10.1). After adjusting for stroke risk factors and number of teeth, controls had higher saliva matrix metalloproteinase-8 (MMP-8), myeloperoxidase (MPO), IL-1β, Aggregatibacter actinomycetemcomitans, and serum LPS activity levels. Patients had higher serum MMP-8 and MPO, and they were more often qPCR-positive for A. actinomycetemcomitans (37.9% versus 19.0%) and for ≥3 periodontopathic species combined (50.0% versus 33.0%). We conclude that controls more often had evidence of current periodontal infection with higher periodontal pathogen amount, endotoxemia, local inflammation and tissue destruction. Stroke patients more often had evidence of end-stage periodontitis with edentulism and missing teeth. They were more often carriers of several periodontopathic pathogens in saliva, especially A. actinomycetemcomitans. Additionally, inflammatory burden may contribute to high systemic inflammation associated with elevated stroke susceptibility.

OBJECTIVE: The replacement of missing teeth with dental implants has been standard practice in dentistry for many years. The success of dental implants depends on many factors, among which the diagnosis, clinical severity, and treatment of peri-implant diseases play a key role. In this prospective case series, the influence of cumulative treatment modalities on peri-implantitis with and without pus formation on clinical outcome was assessed.
METHODS: During 2010, 28 patients were referred for peri-implantitis treatment. They presented two different types of peri-implant diseases: peri-implantitis with (17 implants) or without pus formation (33 implants). After microbiologic diagnosis, all patients were treated at baseline with full-mouth scaling and root planing. Two months later, further full-mouth scaling and root planing and additional antimicrobial photodynamic therapy (aPDT) was applied. Four months after baseline, patients with pus formation additionally underwent access flap surgery. Active human matrix metalloproteinase-8 (aMMP-8) levels were measured in eluates before and after all treatment modalities and 7 months after baseline.
RESULTS: Clinical parameters (probing depth, bleeding on probing) and aMMP-8-levels improved in both groups after treatment and the final examination. In periimplantitis patients without pus formation, all parameters decreased after full-mouth scaling and root planing and the additional aPDT and no surgery was necessary to improve the parameters. In patients with pus formation, the parameters decreased only after access flap surgery.
CONCLUSIONS: The presence of pus influences the clinical outcome of the treatment of peri-implant diseases. Whereas peri-implantitis cases without pus formation can be successfully managed nonsurgically, peri-implantitis with pus formation can be effectively treated after an additional observation time of 3 months postoperatively only with additional flap surgery.