Background. Mucocele is the most common minor salivary glands disease. Its management may present a challenge for dental professionals. The aim of the present clinical case was to describe mucocele treatment with diode laser and its benefits. Case Report. A case of lower lip mucocele in a 10-year-old female patient is reported. A conventional excision surgery was performed. Two months later, the patient reported discomfort and swelling at the same operative site. The lesion had recurred. Thus, mucocele was removed using a diode laser with wavelength of 980 nm, an initiated fiberoptic tip of 300 μm, in continuous mode, and a power setting of 2 Watts. The procedure was rapidly completed with no bleeding. The patient was followed-up after 2 weeks and 6 months. The wound healed without complications: no postoperative discomfort or pain and no infection. There was no recurrence. Conclusion. Diode laser is an effective, easy, bloodless, and well-accepted procedure to treat mucocele in pediatric patients.
Overexpression of the nucleotide-binding leucine-rich repeat protein 3 (NLRP3) inflammasome in chronic auto-immune diseases leads to skeletal anomalies, with severe osteopenia due to the activation of osteoclasts. Reproducing this phenotype in Nlrp3 knock-in mice has provided insights into the role of NLRP3 in bone metabolism. We studied the role of NLRP3 in physiological bone development using a complete Nlrp3 knockout mouse model. We found impaired skeletal development in Nlrp3 −/− mice, resulting in a shorter stature than that of Nlrp3 +/+ mice. These growth defects were associated with altered femur bone growth, characterized by a deficient growth plate and an osteopenic profile of the trabeculae. No differences in osteoclast recruitment or activity were observed. Instead, Nlrp3 −/− femurs showed a less mineralized matrix in the trabeculae than those of Nlrp3 +/+ mice, as well as less bone sialoprotein (BSP) expressing hypertrophic chondrocytes. In vitro, primary osteoblasts lacking NLRP3 expression showed defective mineralization, together with the downregulation of BSP expression. Finally, follow-up by micro-CT highlighted the role of NLPR3 in bone growth, occurring early in living mice, as the osteopenic phenotype diminishes over time. Overall, our data suggest that NLRP3 is involved in bone edification via the regulation of hypertrophic chondrocyte maturation and osteoblast activity. Furthermore, the defect appeared to be transitory, as the skeleton recovered with aging.
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