CO2 Laser De-epithelization Technique for Subepithelial Connective Tissue Graft: A Study of 21 Recessions.

BACKGROUND/AIM: To report cases in which we achieved sufficient width of the keratinized gingiva using a coronally advanced flap in combination with a subepithelial connective tissue graft (SCTG) obtained by the 'CO2 laser de-epithelization technique' (CODE). PATIENTS AND METHODS: Eleven patients with 21 Miller Class I, II, and III gingival recessions had surgery. To prepare SCTG, free gingival grafts were harvested and de-epithelialized extra-orally. De-epithelialization was conducted by irradiation of CO2 laser. Postoperative examinations were performed at 12 months. RESULTS: At 12 months, statistically highly significant root coverage was achieved in all recessions. Complete root coverage was obtained in 7 of the 21 recessions. The treatment yielded mean root coverage of 41.0%, and was associated with a mean gain of keratinized gingiva of 2.9±0.3 mm. CONCLUSION: The use of CODE allows harvesting grafts of excellent quality and quantity and increases the keratinization of the overlying mucosal epithelium.

Methodological quality and risk-of-bias assessments in systematic reviews of treatments for peri-implantitis.

BACKGROUND AND OBJECTIVES: The purpose of the present study was to evaluate the methodological quality and risk of bias in systematic reviews (SRs) on the effectiveness of peri-implantitis treatments. MATERIAL AND METHODS: We searched four electronic databases: MEDLINE, Web of Science, Cochrane Database of Systematic Reviews, and EMBASE. Previous SRs focusing on peri-implantitis treatment published between 2010 and 2017 were identified. After literature screening, eligible SRs were qualitatively assessed using two validated instruments: Assessing the Methodological Quality of Systematic Reviews (AMSTAR2) and Risk Of Bias In Systematic reviews (ROBIS). The characteristics and findings of SRs are also reported. RESULTS: A total of 23 SRs formed the basis of this study. Of the 23, six included randomized controlled trials (RCTs) only. Overall, the AMSTAR2 assessment revealed three studies with high and six studies with low methodological quality, and all the other SRs were judged as having critically low methodological quality. ROBIS revealed only one Cochrane review with a low risk of bias and the others with a high risk of bias. In particular, the assessment of non-randomized studies (NRSIs), appropriateness of ROB assessment, and meta-analysis did not satisfy the criteria in AMSTAR2 assessment. Furthermore, there were a few SRs that interpreted and discussed the results of risk of bias (ROB) and heterogeneity assessment, together with the impact of treatment. CONCLUSIONS: Due to the lack of head-to-head comparisons conducted in RCTs, review authors need to use other sources of evidence, such as clinical control trials (CCTs), cohort studies (CS), clinical research (CR), and animal studies. The end result is the presentation of low-quality evidence, with high ROB. Several SRs conducted network meta-analysis as an alternative to head-to-head conventional meta-analysis of RCTs. We suggest that the best methods to generate, access, and assess evidence in situations where RCT evidence is lacking should be discussed on an urgent basis.

Medullary neural circuit regeneration after trigeminal nerve transection.

The inferior alveolar nerve (IAN) comprises several types of sensory fibers. To clarify whether each type of primary afferent is regenerated comparably after injury, we developed a model of complete IAN transection (IANX) in mice. A retrograde tracer, fluoro-gold, injected into the mental skin was transferred to the cell bodies of a subset of isolectin B4 (IB4)-binding (non-peptidergic C) or CGRP-positive (peptidergic C) neurons at 2 weeks post-axotomy, indicating that the injured C afferents had regenerated anatomically. IANX led to a decrease of IB4-binding and CGRP immunoreactivity (IR) in the trigeminal ganglion (TG) and within the trigeminal spinal subnucleus caudalis (Vc) (i.e. terminals of the central branch of TG neurons). Two weeks after IANX, the reduction in IB4-binding activity and CGRP expression in the TG recovered to the control level; however, IB4-binding within the Vc did not, suggesting that central branch non-peptidergic neurons remained impaired. Two weeks after IANX, pinching or heat stimulus-induced extracellular signal-regulated kinase phosphorylation (pERK) was restored to the control level, but in the case of pinch stimulation the distribution pattern of pERK-IR cells was altered in the Vc. Taken together, our results support the possibility that peptidergic neurons regenerate more efficiently than non-peptidergic neurons after trigeminal nerve injury.

CXCR4 signaling contributes to alveolar bone resorption in Porphyromonas gingivalis-induced periodontitis in mice.

Periodontitis caused by bacterial infection gradually progresses accompanied by periodontal tissue destruction. As a result, teeth lose their supporting structures, and this leads to tooth exfoliation. CXC-chemokine receptor 4 (CXCR4) is known to be expressed in lymphocytes, fibroblasts and osteoclasts in periodontal tissues, suggesting that periodontal CXCR4 signaling contributes to alveolar bone resorption in the milieu of periodontitis. However, the role of CXCR4 signaling in the pathogenesis of periodontitis has remained unknown. We established a mouse model of periodontitis by inoculation of Porphyromonas gingivalis (P.g.) into a silk ligature placed around the maxillary molar. Although there was no significant difference in the mechanical sensitivity in the periodontal tissue between P.g. treatment and sham treatment during the experimental period, mechanical allodynia in the periodontal tissue was induced after gingival injection of complete Freund's adjuvant compared with that resulting from sham and P.g. treatment alone. Moreover, CXCR4 neutralization in the periodontal tissue following P.g. treatment enhanced periodontal inflammatory cell infiltration and depressed alveolar bone resorption. These findings suggest that periodontal CXCR4 signaling in several cell types in P.g.-induced periodontal inflammation depresses alveolar bone resorption in periodontitis. CXCR4 signaling might be a target for therapeutic intervention to prevent alveolar bone resorption in periodontitis.

CXCR4 signaling in macrophages contributes to periodontal mechanical hypersensitivity in Porphyromonas gingivalis-induced periodontitis in mice.

Background Periodontitis is an inflammatory disease accompanied by alveolar bone loss and progressive inflammation without pain. However, the potential contributors eliminating pain associated with gingival inflammation are unknown. Results we examined the involvement of CXC chemokine receptor type 4 (CXCR4) on the mechanical sensitivity of inflamed periodontal tissue, using a mouse model of periodontitis established by the ligation of the tooth cervix of a maxillary second molar and inoculation with Porphyromonas gingivalis (P. gingivalis). Infiltration of inflammatory cells into gingival tissue was not observed following the inoculation. Under light anesthesia, the mechanical head withdrawal threshold (MHWT) on the buccal gingiva was measured using an electronic von Frey anesthesiometer. No significant changes in MHWT were observed in the mice with P. gingivalis-induced periodontitis during the experimental period. Continuous administration of CXCR4 neutralizing antibody to the gingival tissue significantly decreased MHWT and increased the number of gingival CXCR4 immunoreactive macrophages in the periodontitis group. Nitric oxide metabolites in the gingival tissue were significantly increased after the inoculation of P. gingivalis and were reduced by gingival CXCR4 neutralization. Gingival L-arginine administration induced gingival mechanical allodynia in naive animals. Moreover, the decrease in MHWT after treatment with P. gingivalis and CXCR4 neutralization was partially reversed by nitric oxide synthase inhibition in the gingival tissue. Nuclear factor-kappa B was expressed in infiltrating macrophages after inoculation of P. gingivalis and administration of the nuclear factor-kappa B activator betulinic acid induced gingival mechanical allodynia in naive mice. Conclusions These findings suggest that CXCR4 signaling inhibits nitric oxide release from infiltrating macrophages and is involved in modulation of the mechanical sensitivity in the periodontal tissue in P. gingivalis-induced periodontitis.