In recent years there have been an increasing number of in vitro and in vivo studies that show positive results regarding antimicrobial photodynamic therapy (aPDT) used in dentistry. These include applications in periodontics, endodontics, and mucosal infections caused by bacteria present as biofilms. Antimicrobial photodynamic therapy is a therapy based on the combination of a non-toxic photosensitizer (PS) and appropriate wavelength visible light, which in the presence of oxygen is activated to produce reactive oxygen species (ROS). ROS induce a series of photochemical and biological events that cause irreversible damage leading to the death of microorganisms. Many light-absorbing dyes have been mentioned as potential PS for aPDT and different wavelengths have been tested. However, there is no consensus on a standard protocol yet. Thus, the goal of this review was to summarize the results of research on aPDT in dentistry using the PubMed database focusing on recent studies of the effectiveness aPDT in decreasing microorganisms and microbial biofilms, and also to describe aPDT effects, mechanisms of action and applications.

Bone tissue regeneration is a rapidly evolving field aimed at the development of biocompatible materials and devices, such as scaffolds, to treat diseased and damaged osseous tissue. Functional scaffolds maintain structural integrity and provide mechanical support at the defect site during the healing process, while simultaneously enabling or improving regeneration through amplified cellular cues between the scaffold and native tissues. Ample research on functionalization has been conducted to improve scaffold–host tissue interaction, including fabrication techniques, biomaterial selection, scaffold surface modifications, integration of bioactive molecular additives, and post-processing modifications. Each of these methods plays a crucial role in enabling scaffolds to not only support but actively participate in the healing and regeneration process in bone and joint surgery. This review provides a state-of-the-art, comprehensive overview of the functionalization of scaffold-based strategies used in tissue engineering, specifically for bone regeneration. Critical issues and obstacles are highlighted, applications and advances are described, and future directions are identified.

Background: Various procedures have been proposed to treat gingival recession, but few studies compare these procedures to each other. The purpose of this study was to evaluate a clinical comparison of subepithelial connective tissue graft (SCTG) and guided tissue regeneration (GTR) with a collagen membrane in the treatment of gingival recessions in humans.Methods: Twenty‐four defects were treated in 12 patients who presented canine or pre‐molar Miller Class I and/or II bilateral gingival recessions. Both treatments were performed in all patients, and clinical measurements were obtained at baseline and 18 months after surgery. These clinical measurements included gingival recession height (GR), root coverage (RC), probing depth (PD), keratinized tissue width (KT), and final esthetic result.Results: Both SCTG and GTR with a bioabsorbable membrane and bone graft demonstrated significant clinical and esthetic improvement for gingival recession coverage. The SCTG group was statistically significantly better than GTR for height of GR (SCTG = 0.2 mm, GTR = 1.12 mm, P = 0.02) and KT (SCTG = 4.58 mm, GTR = 2.5 mm, P <0.0001). However, PD was statistically significantly better for GTR than SCTG treatment (GTR = 1.66 mm, SCTG = 1.00, P = 0.01). The 2 procedures were statistically similar in root coverage (SCTG = 95.6%, GTR = 84.2%, P = 0.073). The esthetic condition after both treatments was satisfactory (P = 0.024).Conclusions: It was concluded that the gingival recessions treated with the SCTG group were superior for GR, RC, and KT clinical parameters, while GTR demonstrated better PD reduction. The final esthetic results were similar using both techniques. J Periodontol 2000;71:1441‐1447.

Objective: Inflammatory diseases often coincide with reduced bone mass. Mechanoresponsive osteocytes regulate bone mass by maintaining the balance between bone formation and resorption. Despite its biologic significance, the effect of inflammation on osteocyte mechanoresponsiveness is not understood. To fill this gap, we investigated whether the inflammatory cytokines tumor necrosis factor α (TNFα) and interleukin‐1β (IL‐1β) modulate the osteocyte response to mechanical loading.Methods: MLO‐Y4 osteocytes were incubated with TNFα (0.5–30 ng/ml) or IL‐1β (0.1–10 ng/ml) for 30 minutes or 24 hours, or with calcium inhibitors for 30 minutes. Cells were subjected to mechanical loading by pulsatile fluid flow (mean ± amplitude 0.7 ± 0.3 Pa, 5 Hz), and the response was quantified by measuring nitric oxide (NO) production using Griess reagent and by measuring intracellular calcium concentration ([Ca²⁺]_i) using Fluo‐4/AM. Focal adhesions and filamentous actin (F‐actin) were visualized by immunostaining, and apoptosis was quantified by measuring caspase 3/7 activity. Cell‐generated tractions were quantified using traction force microscopy, and cytoskeletal stiffness was quantified using optical magnetic twisting cytometry.Results: Pulsatile fluid flow increased [Ca²⁺]_iwithin seconds (in 13% of cells) and NO production within 5 minutes (4.7‐fold). TNFα and IL‐1β inhibited these responses. Calcium inhibitors decreased pulsatile fluid flow–induced NO production. TNFα and IL‐1β affected cytoskeletal stiffness, likely because 24 hours of incubation with TNFα and IL‐1β decreased the amount of F‐actin. Incubation with IL‐1β for 24 hours stimulated osteocyte apoptosis.Conclusion: Our results suggest that TNFα and IL‐1β inhibit mechanical loading–induced NO production by osteocytes via abrogation of pulsatile fluid flow–stimulated [Ca²⁺]_i, and that IL‐1β stimulates osteocyte apoptosis. Since both NO and osteocyte apoptosis affect osteoclasts, these findings provide a mechanism by which inflammatory cytokines might contribute to bone loss and consequently affect bone mass in rheumatoid arthritis.