The incidence of peri-implantitis for two different implant systems over a period of thirteen years.

OBJECTIVES: To study the incidence of peri-implantitis over 13 years between two types of dental implants. MATERIALS AND METHODS: Peri-implantitis incidence was defined as bone loss ≥ 1.0 mm after 1 year, and with BOP or suppuration. RESULTS: Nineteen subjects with TioBlast AstraTech(™) (AT) and 22 subjects with machine-etched Brånemark Nobel Biocare(®) (NB) implants were studied. The incidences of peri-implantitis between years 1 and 7 and between years 7 and 13 were 26.2% and 7.1% for AT implants, and 30.4% and 11.5% for NB implants (NS). A history of periodontitis was a risk for future incidence of peri-implantitis (Likelihood ratio: 4.1, 95% CI: 2.0, 8.4, p < 0.001). Subjects with a history of systemic disease had a higher incidence of peri-implantitis (p < 0.05). CONCLUSIONS: No difference in the incidence of peri-implantitis over a period of 13 years as an effect implant surface and design was found. Bone loss during the first 7 years after implant installation was greater than thereafter. Microbiological information at year 7 did not predict incidence of peri-implantitis at year 13. Subjects with a previous history of periodontitis and with systemic disease were at higher risk for future incidence of peri-implantitis.

A single-centre randomized controlled clinical trial on the adjunct treatment of intra-bony defects with autogenous bone or a xenograft: results after 12 months.

BACKGROUND: Limited evidence exists on the efficacy of regenerative treatment of peri-implantitis. MATERIAL AND METHODS: Subjects receiving antibiotics and surgical debridement were randomly assigned to placement of autogenous bone (AB) or bovine-derived xenograft (BDX) and with placement of a collagen membrane. The primary outcome was evidence of radiographic bone fill and the secondary outcomes included reductions of probing depth (PD) bleeding on probing (BOP) and suppuration. RESULTS: Twenty-two subjects were included in the AB and 23 subjects in the BDX group. Statistical analysis failed to demonstrate differences for 38/39 variables assessed at baseline. At 12 months, significant better results were obtained in the BDX group for bone levels (p < 0.001), BOP (p = 0.004), PI (p = 0.003) and suppuration (p < 0.01). When adjusting for number of implants treated per subject, a successful treatment outcome PD ≤ 5.0 mm, no pus, no bone loss and BOP at 1/4 or less sites the likelihood of defect fill was higher in the BDX group (LR: 3.2, 95% CI: 1.0-10.6, p < 0.05). CONCLUSIONS: Bovine xenograft provided more radiographic bone fill than AB. The success for both surgical regenerative procedures was limited. Decreases in PD, BOP, and suppuration were observed.

Rheumatoid arthritis and periodontitis - inflammatory and infectious connections. Review of the literature.

UNLABELLED: An association between oral disease/periodontitis and rheumatoid arthritis (RA) has been considered since the early 1820s. The early treatment was tooth eradication. Epidemiological studies suggest that the prevalence of RA and periodontitis may be similar and about 5% of the population are aged 50 years or older. RA is considered as an autoimmune disease whereas periodontitis has an infectious etiology with a complex inflammatory response. Both diseases are chronic and may present with bursts of disease activity. Association studies have suggested odds ratios of having RA and periodontitis varying from 1.8:1 (95% CI: 1.0-3.2, NS) to 8:1 (95% CI: 2.9-22.1, p<0.001). Genetic factors are driving the host responses in both RA and periodontitis. Tumor necrosis factor-α, a proinflammatory cytokine, regulates a cascade of inflammatory events in both RA and periodontitis. Porphyromonas gingivalis is a common pathogen in periodontal infection. P. gingivalis has also been identified in synovial fluid. The specific abilities of P. gingivalis to citrullinate host peptides by proteolytic cleavage at Arg-X peptide bonds by arginine gingipains can induce autoimmune responses in RA through development of anticyclic citrullinated peptide antibodies. In addition, P. gingivalis carries heat shock proteins (HSPs) that may also trigger autoimmune responses in subjects with RA. Data suggest that periodontal therapies combined with routine RA treatments further improve RA status. CONCLUSIONS: Periodontal infection (P. gingivalis) carries a unique risk for development of autoimmune antibodies associated with RA. Patients with RA have either lost many teeth or usually have severe periodontitis. Additional research, both in regards to basic mechanisms as well as clinical studies, are necessary before it can be said that there are causative links between RA and periodontitis. Cross-disciplinary research in well-defined populations should be performed to further enhance knowledge and develop clinical strategies how to coordinate therapy and risk assessments of RA and periodontitis.

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.

Chronic periodontitis, a significant relationship with acute myocardial infarction.

BACKGROUND: Chronic periodontitis (CP) has been associated with cardiovascular diseases. The study purposes were to identify the odds of acute myocardial infarction (AMI) and CP defined at different thresholds. METHODS AND RESULTS: We studied 80 subjects with clinically confirmed AMI and 80 matched control subjects with no evidence of cardiovascular disease all receiving a comprehensive periodontal examination. Statistical analysis demonstrated a difference in the proportion of sites with a periodontal probing depth >/=6.0mm (2.7% for non-AMI and 12.1% for AMI group, 95% CI: -2.8 to 0.01, P<0.05) but no difference in the extent of gingival bleeding was found between groups. The odds ratio of having AMI and periodontitis varied between 9.2:1 to 14.1:1 with the greatest odds ratio if bone loss exceeded 4mm at >/=50% of the teeth (OR: 14.1:1, 95% CI: 5.5 to 28.2, P<0.0001). The odds ratio remained significant also when only non-smokers were considered (51 subjects) (OR: 7.0:1, 95% CI: 2.0 to 24.3, P<0.01). CONCLUSIONS: Our findings suggest that patients who at routine dental visits demonstrate evidence of bone loss around several teeth can predictably be identified as being at risk for future AMI. Such subjects should be referred for medical and periodontal examinations and treatments.