High-frequency near-infrared diode laser provides a high-peak output, low-heat accumulation, and efficient biostimulation. Although these characteristics are considered suitable for osteoarthritis (OA) treatment, the effect of high-frequency near-infrared diode laser irradiation in in vitro or in vivo OA models has not yet been reported. Therefore, we aimed to assess the biological effects of high-frequency near-infrared diode laser irradiation on IL-1β-induced chondrocyte inflammation in an in vitro OA model. Normal Human Articular Chondrocyte-Knee (NHAC-Kn) cells were stimulated with human recombinant IL-1β and irradiated with a high-frequency near-infrared diode laser (910 nm, 4 or 8 J/cm²). The mRNA and protein expression of relevant inflammation- and cartilage destruction-related proteins was analyzed. Interleukin (IL) -1β treatment significantly increased the mRNA levels of IL-1β, IL-6, tumor necrosis factor (TNF) -α, matrix metalloproteinases (MMP) -1, MMP-3, and MMP-13. High-frequency near-infrared diode laser irradiation significantly reduced the IL-1β-induced expression of IL-1β, IL-6, TNF-α, MMP-1, and MMP-3. Similarly, high-frequency near-infrared diode laser irradiation decreased the IL-1β-induced increase in protein expression and secreted levels of MMP-1 and MMP-3. These results highlight the therapeutic potential of high-frequency near-infrared diode laser irradiation in OA.

Maxillary canines require the longest period from the generation of the tooth germ to the completion of eruption, and they have more difficulties in eruption than other teeth. The incisor roots are often resorbed due to malpositioned canines. An 11‐year‐old girl presented with an extremely rare case of root resorption of four maxillary incisors due to bilaterally impacted maxillary canines, which were located excessively mesially. The case was managed through oral surgery and orthodontic treatment over five years. After extracting the maxillary deciduous canines, the maxillary bilateral canines were surgically exposed. The bimaxillary lateral incisors were extracted, and the canines were orthodontically tracted over 8 months. All teeth were then aligned using edgewise brackets. No further root resorption of the central incisors was observed for 5 years after canine traction. This case demonstrates the importance of early detection of abnormally positioned canines.

Temporomandibular joint osteoarthritis (TMJ-OA) is a widespread joint pathology and has a heightened risk of occurring in patients with anterior disc displacement (ADD), suggesting a potential link between disc displacement and TMJ-OA. However, how ADD causes condylar cartilage deformity without excessive loading on the condyle remains unclear. Therefore, in this study, we aimed to investigate the effects of ADD on temporomandibular joint (TMJ) in rats. Twelve-week-old male Wistar rats were randomly assigned to three groups: ADD, sham surgery, and control. A 4-0 silk thread was used to ligate the anterior part of the articular capsule to the posterior part of the zygomatic arch, securing the articular disc 3 mm forward. The ADD and sham groups were sacrificed 4, 6, and 8 weeks after surgery to perform radiological analysis on the TMJ using micro-computed tomography (micro-CT) and histological analyses. CT images of both coronal and sagittal sections revealed bone deformities in the condyles of the ADD group. The obtained images closely resembled the damaged surface of condyles observed in a clinical case of TMJ-OA. Histologically, anterior disc displacement was observed in the ADD group, along with an increase in thickness of the cartilage layer and a reduction in the cartilage matrix within the hypertrophic layer. The expressions of matrix metalloproteinase-13 and alkaline phosphatase were significantly upregulated in the hypertrophic layer and subchondral bone beneath the cartilage layer, indicating that ADD activated cartilage and bone remodeling. This study reported morphological changes of mandibular condyle and histological changes throughout the TMJ and showed that ADD without excessive loading could cause TMJ-OA