Do Intrabony Defects Have a Worse Clinical Response to Step 2 of Periodontal Therapy and Repeated Subgingival Instrumentation Compared with Suprabony Defects? A Systematic Review.

AIM: To assess the differential clinical response to step 2 of periodontal therapy and repeated subgingival instrumentation between teeth with suprabony and intrabony defects. METHODS: Electronic and manual search were performed to identify studies reporting the differential clinical outcomes of non-surgical periodontal therapy (NSPT) in presence or absence of intrabony defects. The Cochrane Risk of Bias 2 and the Newcastle Ottawa scale were used to assess the risk of bias. RESULTS: Two thousand three hundred forty-eight articles were initially screened, and a total of 5 articles were finally included. Regarding the primary outcome measure, two studies reported PPD reduction values at 6 months after step 2 of periodontal therapy, showing an opposite response of intrabony defects compared to suprabony defects (3.2 mm ± 1.9 versus 2.2 mm ± 1.7 and 0.48 mm ± 0.42 versus 0.72 mm ± 0.36, respectively), while one study reported no differences at 3 months. One study showed a negative association between the presence of intrabony defect and PPD reduction at 9 months after non-surgical step 3 (p < 0.05). CONCLUSION: Due to the limited number of studies and heterogeneity of the data, conflicting evidence emerged for the differential response to NSPT of intrabony and suprabony defects.

Safe zones in dorsal portals for wrist arthroscopy: a cadaveric study.

The standard dorsal portals are the most commonly used in wrist arthroscopy. This cadaveric study aims to determine safe zones, by quantitatively describing the neurovascular relationships of the dorsal wrist arthroscopy portals: 1-2, 3-4, midcarpal radial, midcarpal ulnar, 4-5, 6-radial and 6-ulnar. The neurovascular structures of twenty-one fresh frozen human cadaveric upper limbs were exposed, while the aforementioned portals were established with needles through portal sites. The minimum distance between portals and: dorsal carpal branch of radial artery, superficial branch of radial nerve, posterior interosseous nerve and dorsal branch of ulnar nerve, were measured accordingly with a digital caliper, followed by statistical analysis of the data. The median and interquartile range for each portal to structures at risk were determined and a safe zone around each portal was established. Free of any neurovascular structure safe zones surrounding 1-2, 3-4, midcarpal radial, midcarpal ulnar, 4-5, 6-radial and 6-ulnar portals were found at 0.46mm, 2.33mm, 10.73mm, 11.01mm, 10.38mm, 5.95mm and 0.64mm respectively. Results of statistical analysis from comparisons between 1-2, 3-4 and midcarpal radial portals, indicated that 1-2 was the least safe. The same analysis among 3-4, midcarpal radial, midcarpal ulnar and 4-5 portals indicated that midcarpal portals were safer, while 3-4 was the least safe. Results among midcarpal ulnar, 4-5, 6-radial and 6-ulnar portals indicated that 6-radial and specifically 6-ulnar were the least safe. This study provides a safe approach to the dorsal aspect of the wrist, enhancing established measurements and further examining safety of the posterior interosseous nerve.

Prevalence of stable and successfully treated periodontitis subjects and incidence of subsequent tooth loss within supportive periodontal care: A systematic review with meta-analyses.

AIM: To identify (i) the prevalence of meeting the endpoints of 'stable periodontitis' (probing pocket depth [PPD] ≤ 4 mm, bleeding on probing [BoP] < 10%, no BoP at 4 mm sites), 'endpoints of therapy' (no PPD > 4 mm with BoP, no PPD ≥ 6 mm), 'controlled periodontitis' (≤4 sites with PPD ≥ 5 mm), 'PPD < 5 mm' and 'PPD < 6 mm' at the start of supportive periodontal care [SPC]) and (ii) the incidence of tooth loss in relation to not meeting these endpoints within a minimum of 5 years of SPC. MATERIALS AND METHODS: Systematic electronic and manual searches were conducted to identify studies where subjects, upon completion of active periodontal therapy, entered into SPC. Duplicate screening was performed to find relevant articles. Corresponding authors were contacted to confirm inclusion and retrieve required clinical data for further analyses to assess the prevalence of reaching endpoints and incidence of subsequent tooth loss, if available, within at least 5 years of SPC. Meta-analyses were carried out to evaluate risk ratios for tooth loss in relation to not reaching the various endpoints. RESULTS: Fifteen studies including 12,884 patients and 323,111 teeth were retrieved. Achievement of endpoints at baseline SPC was rare (1.35%, 11.00% and 34.62%, respectively, for 'stable periodontitis', 'endpoints of therapy' and 'controlled periodontitis'). Less than a third of the 1190 subjects with 5 years of SPC data lost teeth-a total of 3.14% of all teeth were lost. Statistically significant associations with tooth loss, at the subject-level, were found for not achieving 'controlled periodontitis' (relative risk [RR] = 2.57), PPD < 5 mm (RR = 1.59) and PPD < 6 mm (RR = 1.98). CONCLUSIONS: An overwhelming majority of subjects and teeth do not achieve the proposed endpoints for periodontal stability, yet most periodontal patients preserve most of their teeth during an average of 10-13 years in SPC.

Experimental peri-implantitis around titanium implants with a chemically modified surface with a monolayer of multi-phosphonate molecules: a preclinical in vivo investigation.

OBJECTIVES: The purpose of this experimental in vivo investigation was to evaluate the influence of modifying the implant surface by adding a monolayer of multi-phosphonate molecules on the development of experimental peri-implantitis. MATERIAL AND METHODS: Eight beagle dogs received 5 tests and 5 control implants each following a split-mouth design 3 months after premolar and molar extraction. On the most mesial implant of each side, a 3-mm buccal dehiscence was artificially created. Experimental peri-implantitis was induced by silk ligatures over a 4-month period; after ligature removal, peri-implantitis was left to progress for another 4 months without plaque control. Clinical, histological, and radiographic outcomes were evaluated. RESULTS: Radiographically, both implant groups showed a similar bone loss (BL) at the end of the induction and progression phases. BL measured on the histological sections of the test and control groups was 3.14 ± 0.42 mm and 3.26 ± 0.28 mm, respectively; the difference was not statistically significant (p > 0.05). The remaining buccal bone to implant contact (bBIC) percentage of the test and control groups was 59.38 ± 18.62 and 47.44 ± 20.46%, respectively; the difference, however, was not statistically significant (p > 0.05). Bone loss observed at dehiscent sites compared to non-dehiscent ones showed no statistically significant difference (p > 0.05). CONCLUSIONS: Addition of a monophosphonate layer to a moderately rough implant surface did not affect development of experimental peri-implantitis. CLINICAL RELEVANCE: Influence of implant surface on peri-implantitis may condition implant selection by the clinician, especially on patients with disease risk factors. In that sense, monophosphate layer implants do not show higher peri-implantitis risk than control implants.

Periodontitis, Edentulism, and Risk of Mortality: A Systematic Review with Meta-analyses.

Periodontitis has been independently associated with the chronic noncommunicable diseases that most frequently lead to death worldwide. The aim of the present systematic review was to study whether people with periodontitis/edentulism are at increased risk of all-cause and cause-specific mortality as compared with those without periodontitis/edentulism. Cohort studies were included that 1) evaluated periodontitis or edentulism as exposures in relation to all-cause or cause-specific mortality as an outcome and 2) reported effect estimates as hazard ratios, risk ratios, or odds ratios with 95% CIs or crude numbers. Two review authors independently searched for eligible studies, screened the titles and abstracts, did full-text analysis, extracted the data from the published reports, and performed the risk-of-bias assessment. In case of disagreement, a third review author was consulted. Study results were summarized through random effects meta-analyses. A total of 57 studies were included, involving 48 cohorts and 5.71 million participants. Periodontitis was associated with increased risk of all-cause mortality (risk ratio, 1.46 [95% CI, 1.15 to 1.85]) and mortality due to cardiovascular diseases (1.47 [1.14 to 1.90]), cancer (1.38 [1.24 to 1.53]), coronary heart disease (2.58 [2.20 to 3.03]), cerebrovascular diseases (3.11 [2.42 to 3.98]), but not pneumonia (0.98 [0.69 to 1.38]). Edentulism (all types) was associated with increased risk of all-cause mortality (1.66 [1.46 to 1.88]) and mortality due to cardiovascular diseases (2.03 [1.50 to 2.74]), cancer (1.55 [1.24 to 1.94]), pneumonia (1.72 [1.07 to 2.78]), coronary heart disease (2.98 [2.43 to 3.65]), and cerebrovascular diseases (3.18 [2.24 to 4.51]). Periodontitis and its ultimate sequela (edentulism) are associated with an increased risk of all-cause and cause-specific mortality (PROSPERO CRD42018100095).

Low serum level of 1,25(OH)2 D is associated with chronic periodontitis.

BACKGROUND AND OBJECTIVES: Vitamin D has been studied primarily for its involvement in calcium and phosphate absorption and bone metabolism. The active form of vitamin D-1,25(OH)2 D-has also been investigated for its immune modulatory properties. We explored associations between serum levels of 25(OH)D and 1,25(OH)2 D and periodontal health. SUBJECTS AND METHODS: This case-control study included 55 subjects with chronic periodontitis (cases) and 30 periodontally healthy subjects (controls). Their serum levels of 25(OH)D, 1,25(OH)2 D, ultrasensitive C-reactive protein and high-density lipoprotein cholesterol were determined. Associations between vitamin D and periodontal health status were studied using logistic regression analysis. RESULTS: A statistically significant association was found between serum 1,25(OH)2 D level and periodontal health status; in that subjects with a low 1,25(OH)2 D were more likely to belong to the periodontitis group (OR = 0.97, 95% CI = 0.95-1.00). There was practically no association between 25(OH)D level and periodontal health status. CONCLUSION: In this case-control study low serum 1,25(OH)2 D level appeared to be associated with periodontitis, which was in line with the previously reported associations between serum 1,25(OH)2 D levels and other inflammatory diseases. Whether this association is causal in nature, remains to be confirmed in future studies.