Background: Periodontitis is characterized by alveolar bone destruction; however, the mechanisms responsible for bone damage are poorly understood. It has been reported that T cells are implicated in the pathogenesis of periodontitis. It has been also demonstrated that activated T lymphocytes secrete receptor activator of nuclear factor‐kappa B ligand (RANKL) and can support the differentiation of monocytes into resorbing osteoclasts (OCs). Therefore, the purpose of this study was to examine the OC formation in periodontitis patients (PP) and the role of T cells in osteoclastogenesis.Methods: To study OC formation, we used an in vitro model consisting of unstimulated and unfractionated peripheral blood mononuclear cells (PBMCs) from PP and controls. In parallel, T‐cell–depleted PBMCs from the same patients were also established. The expression of RANKL and tumor necrosis factor‐alpha (TNF‐α) was analyzed by reverse transcription‐polymerase chain reaction (RT‐PCR) and Western blot in fresh T cells isolated from PP and controls. Functional antibodies, anti‐RANKL and anti‐TNF‐α, were utilized to study osteoclastogenesis in PBMC cultures from PP.Results: We showed that, in unfractionated PBMCs from PP, the OCs spontaneously developed in a T‐cell‐dependent way. The addition of macrophage colony stimulating factor (MCSF) and RANKL was necessary to promote the osteoclastogenesis in T‐cell–depleted PBMC cultures from PP and in unfractionated PBMCs from periodontally healthy controls. Moreover, freshly isolated T cells from PBMCs of PP overexpressed RANKL and TNF‐α. Finally, functional anti‐RANKL and anti‐TNF‐α antibodies significantly inhibited osteoclastogenesis.Conclusion: Our data suggest that T cells support spontaneous osteoclastogenesis in PP via RANKL and TNF‐α overexpression.

Several studies have reported the beneficial effects of mesenchymal stem cells (MSCs) in tissue repair and regeneration. New sources of stem cells in adult organisms are continuously emerging; dental tissues have been identified as a source of postnatal MSCs. Dental bud is the immature precursor of the tooth, is easy to access and we show in this study that it can yield a high number of cells with ≥95% expression of mesenchymal stemness makers and osteogenic capacity. Thus, these cells can be defined as Dental Bud Stem Cells (DBSCs) representing a promising source for bone regeneration of stomatognathic as well as other systems. Cell interactions with the extracellular matrix (ECM) and neighboring cells are critical for tissue morphogenesis and architecture; such interactions are mediated by integrins and cadherins respectively. We characterized DBSCs for the expression of these adhesion receptors and examined their pattern during osteogenic differentiation. Our data indicate that N-cadherin and cadherin-11 were expressed in undifferentiated DBSCs and their expression underwent changes during the osteogenic process (decreasing and increasing respectively), while expression of E-cadherin and P-cadherin was very low in DBSCs and did not change during the differentiation steps. Such expression pattern reflected the mesenchymal origin of DBSCs and confirmed their osteoblast-like features. On the other hand, osteogenic stimulation induced the upregulation of single subunits, αV, β3, α5, and the formation of integrin receptors α5β1 and αVβ3. DBSCs differentiation toward osteoblastic lineage was enhanced when cells were grown on fibronectin (FN), vitronectin (VTN), and osteopontin (OPN), ECM glycoproteins which contain an integrin-binding sequence, the RGD motif. In addition we established that integrin αVβ3 plays a crucial role during the commitment of MSCs to osteoblast lineage, whereas integrin α5β1 seems to be dispensable. These data suggest that functionalization of biomaterials with such ECM proteins would improve bone reconstruction therapies starting from dental stem cells.

Introduction. The aim of this study is to demonstrate the effectiveness of addition of the antimicrobial photodynamic therapy to the conventional approach in the treatment of peri-implantitis.Materials and Methods. Forty patients were randomly assigned to test or control groups. Patients were assessed at baseline and at six (T1), twelve (T2), and twenty-four (T3) weeks recording plaque index (PlI), probing pocket depth (PPD), and bleeding on probing (BOP); control group received conventional periodontal therapy, while test group received photodynamic therapy in addition to it.Result. Test group showed a 70% reduction in the plaque index values and a 60% reduction in PD values compared to the baseline. BOP and suppuration were not detectable. Control group showed a significative reduction in plaque index and PD.Discussion. Laser therapy has some advantages in comparison to traditional therapy, with faster and greater healing of the wound.Conclusion. Test group showed after 24 weeks a better value in terms of PPD, BOP, and PlI, with an average pocket depth value of 2 mm, if compared with control group (3 mm). Our results suggest that antimicrobial photodynamic therapy with diode laser and phenothiazine chloride represents a reliable adjunctive treatment to conventional therapy. Photodynamic therapy should, however, be considered a coadjuvant in the treatment of peri-implantitis associated with mechanical (scaling) and surgical (grafts) treatments.

Background: The main therapeutic approach for periodontal diseases is mechanical treatment of root surfaces via scaling and root planing (SRP). Multicenter clinical trials have demonstrated that the adjunctive use of a chlorhexidine (CHX) chip is effective in improving clinical results compared to SRP alone. However, some recent studies failed to confirm these clinical results, and conflicting results were reported regarding the effects of the CHX chip on subgingival microflora. The aim of this study was to provide further data on the clinical and microbiologic effects of CHX chips when used as an adjunct to SRP.Methods: A total of 116 systemically healthy individuals with moderate to advanced periodontitis, aged 33 to 65 years, were recruited from the Departments of Periodontology of four Italian universities. For each subject, two experimental sites were chosen that had probing depths (PD) ≥5 mm and bleeding on probing (BOP) and were located in two symmetric quadrants. These two sites were randomized at the split‐mouth level, with one receiving SRP treatment alone and the other receiving treatment with SRP plus one CHX chip (SRP + CHX). PD, relative attachment level (RAL), and BOP were evaluated at baseline, prior to any treatment, and after 3 and 6 months. Supragingival plaque and the modified gingival index were evaluated at baseline and after 15 days and 1, 3, and 6 months. Subgingival microbiologic samples were harvested at baseline and after 15 days and 1, 3, and 6 months, cultured for total bacterial counts (TBCs), and investigated by polymerase chain reaction analysis for the identification of eight putative periodontopathogens.Results: When all of the pockets were considered, the PD and RAL were significantly less at 3 and 6 months compared to the baseline scores (P <0.01) for both treatments. Moreover, the PD was reduced in the SRP + CHX treatment group compared to the SRP treatment group at 3 and 6 months, whereas the RAL was similar for both treatments at 3 months and was reduced in the SRP + CHX treatment group at 6 months. The differences in PD reductions between the treatments were 0.30 and 0.55 mm at 3 and 6 months, respectively (P <0.01); for the RAL gain, the differences were 0.28 and 0.64 mm, respectively (P <0.001). The TBCs decreased significantly with both treatments. A similar, although less evident, pattern was noted when only the pockets with an initial PD ≥7 mm were considered. The percentage of sites positive for BOP was similar between the treatments at each time point. At 15 days and 1 month, the TBC for the SRP + CHX treatment group was significantly lower than for the SRP treatment group (P <0.01 and P <0.05, respectively). Over time, both treatments generally reduced the percentages of sites positive for the eight putative periodontopathic bacteria, although greater reductions were seen often for the SRP + CHX treatment group.Conclusions: The adjunctive use of the CHX chip resulted in a significant PD reduction and a clinical attachment gain compared to SRP alone. These results were concomitant with a significant benefit of SRP + CHX treatment on the subgingival microbiota.