Soft tissue substitutes in non-root coverage procedures: a systematic review and meta-analysis.

OBJECTIVES: The present systematic review compared the effectiveness of soft tissue substitutes (STSs) and autogenous free gingival grafts (FGGs) in non-root-coverage procedures to increase keratinized tissue (KT) width around teeth. MATERIALS AND METHODS: Included studies fulfilled the following main eligibility criteria: (a) preclinical in vivo or human controlled trials using FGG as control, (b) non-root-coverage procedures, and (c) assessment of KT width. Meta-analysis was performed on the gain in KT width (primary outcome variable) and several secondary variables. RESULTS: Eight human trials with short observation time evaluating five different STSs were identified. FGG yielded consistently significantly (p < 0.001) larger increase in KT width irrespective whether the comparison regarded an acellular matrix or a tissue-engineered STS. Further, FGG yielded consistently ≥2 mm KT width postoperatively, while use of STS did not, in the few studies reporting on this outcome. On the other hand, STSs resulted in significantly better aesthetic outcomes and received greater patient preference (p < 0.001). CONCLUSIONS: Based on relatively limited evidence, in non-root-coverage procedures, FGG (1) resulted consistently in significantly larger increase in KT width compared to STS and (2) yielded consistently ≥2 mm KT width postoperatively, while STSs did not. STSs yielded significantly better aesthetic outcomes, received greater patient preference, and appeared safe. CLINICAL RELEVANCE: Larger and more predictable increase in KT width is achieved with FGG, but STSs may be considered when aesthetics is important. Clinical studies reporting relevant posttreatment outcomes, e.g., postop KT width ≥2 mm, on the long-term (>6 months) are warranted.

Periimplantitis Treatment: Long-Term Comparison of Laser Decontamination and Implantoplasty Surgery.

PURPOSE: Periimplantitis is the most frequent cause of late implant failure; however, little is known about the long-term success of periimplantitis treatment and the effectiveness of various therapeutic interventions. MATERIALS AND METHODS: A total of 142 patients were referred to the Academy for Oral Implantology in Vienna for the treatment of recurrent periimplantitis around single-tooth implants. Of them, 72 patients (51%) were treated by laser decontamination, 47 patients (33%) by implantoplasty surgery, and 23 patients (16%) by a combination of both approaches. RESULTS: Overall success of periimplantitis therapy was 89% after 9 years of follow-up, and it did not differ significantly between female and male patients (P = 0.426). The number of implant failures that could not be prevented by periimplantitis treatment was 6 after laser decontamination (8%), 6 after implantoplasty surgery (13%), and 4 after a combination of both therapies (17%). Implant loss occurred after 4.9 ± 1.9 years of therapy, on average. No significant difference between the 3 treatment groups could be observed (P = 0.393). CONCLUSION: The present results suggest that success rates of periimplantitis therapy with either laser decontamination or surgical implantoplasty are high. These success rates do not appear to be associated with patient gender or treatment strategy.

Soluble CD14 Enhances the Response of Periodontal Ligament Stem Cells to P. gingivalis Lipopolysaccharide.

Periodontal ligament stem cells (PDLSCs) are lacking membrane CD14, which is an important component of lipopolysaccharide (LPS) signaling through toll-like receptor (TLR) 4. In the present study we investigated the effect of soluble CD14 on the response of human PDLSCs to LPS of Porphyromonas (P.) gingivalis. Human PDLSCs (hPDLSCs) were stimulated with P. gingivalis LPS in the presence or in the absence of soluble CD14 (sCD14) and the production of interleukin (IL)-6, chemokine C-X-C motif ligand 8 (CXCL8), and chemokine C-C motif ligand 2 (CCL2) was measured. The response to P. gingivalis LPS was compared with that to TLR4 agonist Escherichia coli LPS and TLR2-agonist Pam3CSK4. The response of hPDLSCs to both P. gingivalis LPS and E. coli LPS was significantly enhanced by sCD14. In the absence of sCD14, no significant difference in the hPDLSCs response to two kinds of LPS was observed. These responses were significantly lower compared to that to Pam3CSK4. In the presence of sCD14, the response of hPdLSCs to P. gingivalis LPS was markedly higher than that to E. coli LPS and comparable with that to Pam3CSK4. The response of hPdLSCs to bacterial LPS is strongly augmented by sCD14. Local levels of sCD14 could be an important factor for modulation of the host response against periodontal pathogens.

Inter- and intra-observer agreement on Miller's classification of gingival tissue recessions.

Miller's is the most commonly used classification of gingival tissue recessions, defined as the displacement of the soft tissue margin apical to the cemento-enamel junction. However, data on the reliability of this classification are missing so far, although reliability, which reflects the consistency of repeated measurements, is regarded as a prerequisite for judging the utility of a classification. The aim of the present study was to evaluate inter- and intra-observer agreement on Miller's classification of gingival tissue recessions. Two hundred photographs (50 of each region: maxillary/mandibular anterior/posterior teeth) of gingival tissue recessions were evaluated twice by four observers with different degrees of experience in Miller's classification, gingival phenotype, tooth shape, and identifiability of the cemento-enamel junction. The following inter- and intra-observer agreements were found: Miller's classification, 0.72 and 0.73-0.95; gingival phenotype, 0.29 and 0.45-0.58; tooth shape, 0.39 and 0.44-0.59; and identifiability of the cemento-enamel junction, 0.21 and 0.30-0.59. A higher agreement was detected for anterior teeth. Further, gingival phenotype (thin-high scalloping) significantly correlated with tooth shape (long-narrow) (ρ = 0.662, p < 0.001). Miller's classification of gingival tissue recessions was evaluated by four examiners using 200 clinical photographs and yielded substantial to almost perfect agreement, with higher agreement for anterior teeth. Although limited to photographic assessment, the present study offers the so far missing proof on the sufficient inter- and intra-observer agreement of this classification.

Total Antioxidant Capacity and Total Oxidant Status in Saliva of Periodontitis Patients in Relation to Bacterial Load.

The detection of salivary biomarkers has a potential application in early diagnosis and monitoring of periodontal inflammation. However, searching sensitive salivary biomarkers for periodontitis is still ongoing. Oxidative stress is supposed to play an important role in periodontitis progression and tissue destruction. In this cross-sectional study, we investigated total antioxidant capacity (TAC) and total oxidant status (TOS) in saliva of periodontitis patients compared to healthy controls and their relationship with periodontopathic bacteria and periodontal disease severity. Unstimulated saliva was collected from 45 patients with generalized severe periodontitis and 37 healthy individuals and the TAC/TOS were measured. In addition, salivary levels of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Fusobacterium nucleatum in saliva were measured. Salivary TAC was lower in periodontitis patients compared to healthy controls. Moreover, a significant negative correlation of salivary TAC with clinical attachment loss was observed in periodontitis patients. No significant difference in the salivary TOS was observed between periodontitis patients and healthy controls. Bacterial load was enhanced in periodontitis patients and exhibited correlation with periodontal disease severity but not with salivary TAC/TOS. Our data suggest that changes in antioxidant capacity in periodontitis patients are not associated with increased bacterial load and are probably due to a dysregulated immune response.