[Healing effect of photodynamic therapy on extraction sockets of periodontally compromised teeth: a randomized, controlled, superiority clinical trial].

Objective: To evaluate the effects of photodynamic therapy (PDT) in extraction sockets of periodontally compromised molars on soft tissue healing, postoperative pain, bone density and bone height changes. Methods: This study is a single-center, single-blind, randomized controlled superiority clinical trial. Thirty-eight periodontally compromised molars requiring extraction in patients attending the Department of Periodontology, Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, from December 2022 to September 2023 were included, and randomly assigned to PDT group and control group. The control group received routine debridement after extraction, while PDT group received routine debridement followed by PDT. The bucco-lingual and mesio-distal wound distances at 7 and 14 d after extraction were measured, and then the wound closure rates were calculated. Evaluating the soft tissue healing indexes at 7 and 14 d after extraction. The visual analogue scale was used to assess the pain level at 6 h, 1 d, 2 d, and 3 d after tooth extraction. Apical radiographs were taken immediately and 2 months after extraction in order to compare the changes of the bone density and height. Results: The wound closure rate at 1 week was (78.08±5.45)% in PDT group and (71.03±6.82)% in control group, with significant differences (P<0.01). The wound closure rate at 2 weeks in PDT group [(85.88±3.84) %] was significantly higher than that in the control group [(81.66±3.79) %] (P<0.01), but did not reach the superiority value of the superiority test (superiority value=10%, 95%CI at 1 week: 3.00%-11.12%, 95%CI at 2 weeks: 1.71%-6.73%). The soft tissue healing index of PDT group at 1 week was significantly better than the control group (P<0.05), but there was no significant difference between the two groups at 2 weeks (P>0.05). There was no significant difference between the two groups in terms of postoperative pain at 6 h, 1 d, 2 d and 3 d as well as in bone density and height changes at 2 months after tooth extraction (P>0.05). Conclusions: PDT could promote soft tissues healing to some extent, but did not provide additional assistance in the healing of extraction sockets of periodontally compromised teeth. PDT did not show benefits on postoperative pain, changes of the bone density and bone height after tooth extraction.

Casp11 Deficiency Alters Subgingival Microbiota and Attenuates Periodontitis.

Periodontitis (PD) is the primary cause of tooth loss in adults. Porphyromonas gingivalis (P.g), a keystone pathogen, has been identified as a crucial contributor to this process. Pyroptosis activation in PD is acknowledged, with accumulating evidence underscoring the crucial role of Caspase-11 (described as Caspase-4/5 in humans)-mediated noncanonical pyroptosis. However, the mechanism behind its impact on PD remains unclear. In this study, we delved into the interplay between the Caspase-11-mediated noncanonical pyroptosis, subgingival microbiota alteration, and macrophage polarization. Clinical samples from PD patients revealed heightened expression of Caspase-4, gasdermin-D, and their active fragments, pointing to the activation of the noncanonical pyroptosis. Single-cell sequencing analysis linked Caspase-4 with gingival macrophages, emphasizing their involvement in PD. In vitro cell experiments confirmed that P.g-induced pyroptosis was activated in macrophages, with Casp11 deficiency attenuating these effects. In an experimental PD mouse model, Casp11 deficiency led to an alteration in subgingival microbiota composition and reduced alveolar bone resorption. Casp11-/- mice cohousing with wild-type mice confirmed the alteration of the subgingival microbiota and aggravated the alveolar bone resorption. Notably, Casp11 deficiency led to decreased M1-polarized macrophages, corresponding with reduced alveolar bone resorption, uncovering a connection between subgingival microbiota alteration, macrophage M1 polarization, and alveolar bone resorption. Taken together, we showed that Caspase-11 fulfilled a crucial role in the noncanonical pyroptosis in PD, potentially influencing the subgingival microbiota and linking to M1 polarization, which was associated with alveolar bone resorption. These findings underscored the pivotal role of the Caspase-11-mediated noncanonical pyroptosis in PD pathogenesis and may provide critical insights into potential therapeutic avenues for mitigating PD.