Background: Sleep bruxism (SB) is a prevalent yet often undetected condition encountered in dental practice, primarily known for its dental consequences such as tooth wear and fracture. While typically regarded as a benign physiological behavior in healthy individuals, a growing body of research suggests that SB may be associated with various medical or sleep-related disorders in certain contexts. This evolving understanding highlights the need for a more integrated, multidisciplinary approach to its assessment and management. Objective: This narrative review aims to explore the associations between SB and various medical and sleep-related conditions. Special attention is given to its relationship with obstructive sleep apnea (OSA), the most extensively studied comorbidity. Methods: A targeted literature search was conducted via PubMed (November 2023-June 2024) using the keywords related SB and its comorbidities. Studies involving adults and addressing the association between SB and OSA, restless leg syndrome (RLS), periodic limb movement disorder (PLMD), insomnia, epilepsy, gastroesophageal reflux disease (GERD), rapid eye movement (REM) sleep behavior disorder (RBD), and Parkinson's disease (PD) were reviewed. Results: The SB-OSA relationship has been the most extensively studied. While many studies suggest a temporal and arousal-based link, findings remain mixed due to variability in diagnostic criteria, methodology, and differentiation from non-specific oromotor activity. Possible associations with RLS and PLMD may reflect shared arousal-related mechanisms, with dopaminergic involvement. While in epilepsy, SB likely reflects arousal-activated motor activity. GERD may trigger SB as a protective salivary reflex, and SB during REM sleep may be relevant in RBD and PD. Evidence for an insomnia remains inconclusive and may be indirectly influenced by psychological distress. Conclusions: Although SB is generally benign, its co-occurrence with specific comorbidities may signal underlying disorders. Recognizing these associations is essential for distinguishing physiological from pathological SB and for guiding appropriate interdisciplinary clinical decision-making.

Purpose: Galleria mellonella has gained recognition as a promising in vivo model for studying bacterial virulence due to its cost-effectiveness, ease of handling, and ethical advantages over vertebrate models. This study explored the feasibility of utilizing G. mellonella to assess strain-specific differences in the virulence of periodontal pathogens. Materials and Methods: Larvae were injected with different Prevotella intermedia and Porphyromonas gingivalis strains, including wild-type and mutant forms, and survival rates were recorded for 72 hours. Kaplan-Meier survival curves were plotted, and statistical tests were conducted to assess significant differences in virulence. The fimA-deficient (KDP150) and rgpB-deficient (G102) P. gingivalis mutants were included to evaluate the contributions of fimbriae and gingipains to bacterial pathogenicity. Results: Survival analysis revealed significant differences in the virulence of P. intermedia strains, with ATCC 49046 exhibiting the highest pathogenicity and ATCC 25611 the lowest. Strains ATCC 15032, ATCC 15033, and 17 displayed intermediate levels of virulence. In P. gingivalis, the fimA-deficient mutant exhibited markedly lower virulence than the wild-type strain, whereas the rgpB-deficient mutant did not show a notable decrease in pathogenicity. These findings suggest that fimbriae play a critical role in P. gingivalis virulence, whereas RgpB protease may be functionally redundant due to compensatory mechanisms. Conclusion: This study demonstrated that G. mellonella can serve as a reliable model for evaluating strain-level differences in the virulence of periodontal pathogens. It effectively distinguished variations among P. intermedia strains and highlighted the role of specific virulence factors in P. gingivalis, supporting its use as an ethical and practical alternative to vertebrate models in oral infection research.

Purpose: Mitochondria transplantation has emerged as a promising strategy to restore cellular function in mitochondrial dysfunction-related disorders. However, the therapeutic efficacy of transplanted mitochondria may vary depending on their tissue of origin. This study aimed to investigate whether mitochondria derived from different donor cell types exert distinct effects on osteoblast differentiation. Materials and Methods: Primary osteoblasts were isolated from neonatal mouse calvariae, while primary myoblasts and fibroblasts were obtained from adult mouse skeletal muscle using enzymatic digestion and pre-plating techniques. Extracellular mitochondria were collected from the conditioned media of differentiating osteoblasts, while intracellular mitochondria were isolated from homogenized myoblasts and fibroblasts using differential centrifugation. Mitochondria from each source were transplanted into primary calvarial osteoprogenitor cells cultured in osteogenic differentiation media. Osteoblast differentiation was assessed three days post-transplantation via alkaline phosphatase (ALP) staining and quantitative RT-PCR for Alpl expression. Results: Osteoblast-secreted mitochondria significantly enhanced osteogenic differentiation, as shown by increased ALP activity and elevated Alpl gene expression. In contrast, mitochondria derived from myoblasts and fibroblasts significantly suppressed osteogenic differentiation. Myoblast-derived mitochondria had a more pronounced inhibitory effect compared to fibroblast-derived mitochondria. These findings confirm that the origin of mitochondria has a critical impact on promoting osteogenesis through mitochondria transplantation. Conclusion: Our study demonstrates that mitochondria from different donor cell types differentially affect osteoblast differentiation. Osteoblast-secreted mitochondria promote osteogenesis, while myoblast- and fibroblast-derived mitochondria suppress it. Our findings underscore the importance of selecting an appropriate mitochondrial source for transplantation and suggest that osteoblast-secreted mitochondria may be a promising therapeutic strategy for the regeneration of hard tissues such as bone or dentin.