The field of tissue engineering is transitioning from bioinert to bioactive materials that actively regulate host biology. Here, we developed a 3D-printed porous Ti scaffold infiltrated with molten Zn to form an interpenetrating Ti/Zn composite with immunomodulatory and osteogenic bioactivity. Corrosion characterization revealed sustained and stable Zn2+ release. In vivo evaluation using a rat rib implantation model confirmed enhanced peri-implant bone regeneration, accompanied by localized Ca/P deposition at Zn degradation sites, indicating biofunctionally favorable degradation. In vitro, Ti/Zn extract induced a shift toward an anti-inflammatory M2 macrophage phenotype. Mechanistically, Zn2+ altered intracellular Ca2+ dynamics, elevating cytoplasmic Ca2+ while preventing mitochondrial Ca2+ overload, thereby preserving mitochondrial membrane potential and inner membrane protein complex stability. This Ca2+ redistribution selectively activated ERK/MAPK signaling, linking ionic cues to mitochondrial homeostasis, reduced ROS generation, and suppression of cytochrome c-mediated intrinsic apoptosis. The immunoregulatory secretome from Ti/Zn-reprogrammed macrophages further promoted osteoblast proliferation, ALP activity, and osteogenic gene/protein expression. In vivo immunohistochemistry and immunofluorescence validated a remodeled immune microenvironment with attenuated oxidative stress and active new bone synthesis. Overall, the Ti/Zn composite integrates bone-mimetic architecture with ion-driven immunometabolic regulation, highlighting its potential as a next-generation bioactive bone implant.

Denosumab is a humanized monoclonal antibody targeting receptor activator of nuclear factor-κB ligand(RANKL)and is commonly used in the treatment of osteoporosis and cancer-related bone metastases.However,the per-sistent use of denosumab has been associated with an increasing incidence of denosumab-related osteonecrosis of the jaw(DRONJ),particularly following tooth extraction.This expert consensus aims to develop clinical management guidelines for the perioperative period of tooth extraction in patients who are currently receiving or have previously received deno-sumab therapy.The consensus covers the definition,etiology,epidemiology,staging,and risk factors of DRONJ,focus-ing on preoperative assessment,risk-based prevention strategies,minimally invasive surgical techniques,and postopera-tive follow-up protocols.The core management strategy for DRONJ emphasizes individualized decision-making based on a comprehensive preoperative assessment of medication history,local infection,and systemic conditions.The main risk factors for DRONJ include high-dose and long-term denosumab therapy,preexisting oral infections,such as peri-odontitis and periapical periodontitis,and invasive dental procedures,including tooth extraction,diabetes,and concomi-tant use of glucocorticoids or antiangiogenic agents.Core preventive measures include strict perioperative oral care,risk assessment-based antibiotic prophylaxis,long-term drug holidays,which were developed by dentists and physicians prio-ritizing the primary disease,and minimally invasive surgical techniques for managing trauma,preserving local blood sup-ply,thoroughly removing infected tissues,and ensuring tight wound closure.This consensus highlights the importance of multidisciplinary collaboration between dental and clinical medicine experts in managing DRONJ.High-quality research is necessary to provide an evidence-based foundation for optimizing DRONJ prevention and treatment strategies.

Arsenic exposure increases the risk of bladder cancer. The proteomic analysis of arsenic treated bladder epithelial cells revealed significantly upregulated NMES1 expression, which was further validated in the bladder epithelium of arsenite-exposed mice and SV-HUC-1 cells treated with 0.5 μM arsenite. NMES1 is a nuclear-encoded accessory protein of mitochondrial respiratory chain complex IV. A direct interaction between ALKBH7 and NMES1 was confirmed by both molecular docking and protein interaction assays. ALKBH7, a mitochondrial RNA demethylase, was significantly downregulated in arsenic-exposed bladder epithelial cells. Arsenic-mediated ALKBH7 inhibition elevated the m22G methylation level of tRNAs flanking in the mitochondrial respiratory chain, accompanied by decreased mRNA levels of lysine, arginine, and glycine, as well as reduced protein expression of mt-CO2 and mt-ND3, ultimately causing mitochondrial respiratory dysfunction. In addition, arsenic exposure also enhanced cellular glycolysis, which provides energy support for the proliferation and migration of bladder epithelial cells. siNMES1 alleviated arsenic-induced ALKBH7 downregulation and cell malignant phenotype. Overexpressed ALKBH7 effectively attenuated arsenic-enhanced glycolysis and malignant phenotype. In conclusion, arsenic upregulates NMES1 to suppress ALKBH7 expression that increased mt-tRNA m22G methylation modification and reduces the expression of the mt-CO2 and mt-ND3 subunits, thereby impairing mitochondrial respiratory function. Inhibiting ALKBH7 further promoted glycolytic reprogramming to sustain malignant phenotypes in arsenic treated bladder epithelial cells.

Mesenchymal stem cell (MSC)-based therapies present substantial opportunities for regenerative medicine, yet the absence of lineage-specific tools for precise cell recruitment constitutes a primary limitation. In this study, we developed a novel ssDNA aptamer, designated as Pt-1, specifically evolved against human dental pulp stem cells (hDPSCs) using Cell-SELEX technology. Pt-1 exhibited high target specificity, strong binding affinity, and favorable physiological stability. Notably, Pt-1 identified a distinct subpopulation within heterogeneous DPSCs; the Pt-1high subset displayed significantly enhanced proliferative capacity and osteo/odontogenic potential compared to the Pt-1Low group. Through proteomic analysis and molecular docking, we elucidated that Pt-1 recognizes Cav1-associated target as its membrane target. To translate this molecular recognition into a regenerative strategy, we engineered a Pt-1-functionalized ChSMA hydrogel. This bio-instructive scaffold demonstrated superior efficacy in orchestrating the homing of endogenous MSCs in vitro and in vivo compared to the established Apt19S aptamer. In rat models of dental pulp and femoral bone defects, the Pt-1-modified hydrogel significantly accelerated tissue restoration, promoting more mature trabecular bone formation and pulp tissue regeneration. In summary, we developed a novel ssDNA aptamer targeting MSCs and established an aptamer-based strategy for precise endogenous cell recruitment, opening new therapeutic avenues for regenerative medicine.

Traditional calcium-based materials often fail in clinical bone repair due to poor vascularization and tissue integration. To address this, we developed a "vascular homeostasis-bone regeneration" strategy using a ternary coacervate system composed of tannic acid (TA), gelatin, and polyethylene glycol to encapsulate amorphous calcium phosphate (ACP). This TGP@ACP system combines moldable wet-adhesion with controlled ion release and potent antioxidant properties. In vitro, the coacervate significantly enhanced both osteogenic and angiogenic activities. In a rat cranial defect model, TGP@ACP increased type H vessel density by 9.5-fold and bone volume by 4.9-fold compared to untreated controls. Single-cell RNA sequencing revealed that the system stabilizes nascent vessels by improving mitochondrial homeostasis and upregulating tight junction proteins in endothelial cells. Finally, the therapeutic efficacy was validated in a beagle mandibular defect model, where TGP@ACP successfully restored alveolar ridge morphology. This dual-functional system offers a promising clinical solution for complex bone defect repair by synergistically promoting angiogenesis and osteogenesis.

The third molar is the most developmentally delayed of the permanent teeth and has the highest incidence of pericoronitis and odontogenic space infections. Impacted third molars significantly increase the risk of periodontitis, dental caries, and external root resorption of adjacent second molars. Third molars are associated with complex surgical procedures, and treatment decisions and clinical management of third molars in this context remain controversial. This expert consensus was generated by oral surgeons and related specialists, who synthesized the current evidence-based literature and contemporary clinical practices. This consensus addresses critical considerations: the developmental trajectory and impaction characteristics of third molars, clinical and radiographic examinations of third molars, classification of impacted third molars, adverse effects of impacted third molars on oral health, indications for extraction, preoperative preparation for impacted third molar removal, anesthetic choices for impacted third molar surgery, recommended surgical protocol for impacted third molar removal, application of implant materials in alveolar sockets, management of common severe complications in impacted third molar extraction, and functional utilization of impacted third molars. Based on a comprehensive expert deliberation, this consensus provides evidence-based clinical guidance and standardized protocols for dental practitioners in the context of third molar management and therapeutic decision-making.

Restoring the natural structure and morphology of alveolar bone remains a significant clinical challenge in bone defect repair. Recent studies have emphasized the critical role of the structural features of biomaterials in regulating the organized arrangement of stem cells during the repair of critical-size bone defects. Inspired by the aligned structure of the lamellar bone extracellular matrix (ECM), anisotropic gelatin methacryloyl/oxidized chitosan hydrogels (referred to as GelMA-2%OC-T) were developed by employing directional freeze-casting combined with mechanical training, consisting of well-aligned fibrous structures. The fracture toughness of the GelMA-2%OC-T hydrogels in the Y-direction (0.96 MJ/m(3)) was similar to 3.8 times that of the X-direction (0.25 MJ/m(3)). GelMA-2%OC-T samples demonstrated excellent biocompatibility, effectively guiding the oriented alignment of neural crest-derived stem cells (NCSCs) when seeded for 24 h, and promoted osteogenic differentiation in vitro by activating the ITGA7-COL1A1 axis, as revealed by transcriptome sequencing. Implantation of GelMA-2%OC-T scaffolds into rabbit alveolar bone defects for 8 weeks facilitated new bone formation and restored the original structure and morphology of the alveolar bone. Thus, this study offers a novel strategy for designing artificial biomaterials by mimicking the aligned structure of the lamellar bone ECM aimed at directing bone regeneration and restoring natural structures.

Arsenic exposure by drinking water is a key challenge in the field of public health worldwide. Research has found a connection between arsenic exposure and renal fibrosis, yet the mechanisms behind this are still unclear. In this study, rats were exposed to 50 mg/L NaAsO2 or 200 mg/L dimethylarsinic acid (DMA) via drinking water for 12 weeks, and HK-2 cells were treated with 1 μM NaAsO2 for 4 weeks. The results showed that the renal tubular structure was destroyed, renal function was impaired, and fibrosis occurred in renal tissue in arsenic-exposed F344 rats. Arsenic-treated HK-2 cells presented hydroxyproline levels elevating and fibrosis-related proteins expression increasing. In addition, the levels of Hedgehog signaling pathway-related factors SMO, SHH, GLI1, GLI2 were increased and SUFU was decreased in kidneys of arsenic-treated rats and HK-2 cells, indicating that the Hedgehog signaling pathway was triggered. The fibrosis level was reduced in arsenic treated HK-2 cells after interference with the Hedgehog pathway inhibitor. The activity of GLI1, an important factor in the Hedgehog signaling pathway, is regulated by acetylation modifications. Levels of GLI1 acetylation were reduced in arsenic treated HK-2 cells1. In conclusion, the Hedgehog signaling pathway is vital in arsenic-triggered renal fibrogenesis.

Titanium (Ti) alloys are widely used in bone repair due to their excellent biocompatibility and mechanical properties. However, managing post-implantation inflammatory responses in the defect region and accelerating the healing process remain major challenges in the design of such materials. As a bridge between the innate and adaptive immune systems, macrophages play a pivotal role in bone defect healing through their M2 polarization, which facilitates the secretion of tissue repair-promoting cytokines. Research on the role of copper ions (Cu²⁺) in regulating inflammatory responses at injury sites suggests their potential as active ions for incorporation into alloys as a secondary phase to modulate macrophage polarization. However, the effective concentration and mechanisms in this process remain unclear. Here, we synthesized Ti-xCu (x = 3, 5, 7 wt%) alloys and investigated the effects of copper concentration on macrophage M1/M2 polarization and the underlying mechanisms. In an 8-week rat mandibular bone regeneration experiment, Ti-5Cu demonstrated superior performance compared to pure titanium. At the early stage (2 weeks), Ti-5Cu promoted the dominance of M1 macrophages and upregulated inflammatory cytokines, facilitating the initial inflammatory response. Subsequently, a timely M1-to-M2 phenotype transition was observed, accompanied by elevated expression of the repair-related cytokine IL-10, ultimately leading to improved bone healing. This study provides a theoretical foundation for the development of titanium-copper composite materials with anti-inflammatory and pro-healing properties, paving the way for innovative solutions to promote bone defect repair.

Chronic exposure to arsenic via drinking water can induce bladder cancer in humans. Nevertheless, there is little knowledge about the precise mechanisms of this. Abnormal elevations in cell proliferation and migration have repeatedly been identified as the first cellular traits of carcinogenesis. The aims of this study are to uncover the molecular mechanisms underlying arsenic-induced aberrant proliferation and migration of uroepithelium cells by exploring the role of cellular redox modulation. Our results show significant elevations in the levels of ROS and GSH, Trx1, components of the Nrf2 system, and NLRP3 inflammasome activity in the cells chronically treated with arsenite, which also experienced markedly enhanced proliferation and migration capacities. Additionally, ROS inhibitors, NLRP3, and the above antioxidant system could suppress this enhancement of the proliferation and migration capacities and reverse overexpression in these cells. However, only the AKT and ERK inhibitors were capable of reversing EGF, TGFα, and HSP90 overexpression. In conclusion, our findings indicate that the cellular redox status in the uroepithelium following chronic treatment with low-level arsenite was rebalanced due to ROS overproduction and compensatory upregulation of the redox control systems, which may allow ROS and Trx1 to be maintained at higher levels to facilitate cell proliferation and migration via overstimulation of the related signaling pathways.

Guided bone regeneration in the alveolar bone relies on the colonization and differentiation of immune cells within the defect area. The absence of osteoinductive and osteoimmune properties of currently available scaffolds hinders to achieve optimal repair outcomes in clinical settings. Thus, we aimed to enhance the bone repair ability of polycaprolactone (PCL) scaffolds by incorporating osteoinductive amorphous calcium phosphate (ACP) with immune-regulating zinc ions (ACP(Zn), ACZP), to create a favorable immunomodulatory microenvironment. After one day of co-culture with PCL-ACZP, the spreading area of macrophage cells was significantly higher than that from the original PCL scaffold. Additionally, over 32.1 % of macrophages exhibited M2 polarization within three days of co-culture. The PCLACZP/macrophage-conditioned medium significantly boosted osteogenic gene expression in MC3T3-E1 cells. After eight weeks of implantation in a rat femoral condyle defect, the BV/TV from the PCL-ACZP group reached 32.9 %, 1.4 times of that from the PCL group. Furthermore, the PCL-ACZP-GelMA biphasic module as prepared successfully achieved complete regeneration of three-walled alveolar bone defects in rabbits, resulting in arch-shaped alveolar bone repair and providing greater convenience in the clinical settings. This study showcased the effectiveness of PCL-ACZP-GelMA biphasic module as bioactive scaffolds in the morphological restoration of alveolar bone. (c) 2025 Published by Elsevier Ltd on behalf of The editorial office of Journal of Materials Science & Technology.

Arsenic is a widespread global pollutant, and its exposure increases the risk of bladder cancer. However, the exact mechanism involved is still unclear. Here, we explored the mechanisms of arsenic-induced lipid metabolism reprogramming in malignant phenotypes, focusing on the regulatory role of acylglycerol-acyltransferase 1 (DGAT1), a key enzyme in the final step of triglyceride synthesis. The effects of continuous exposure to arsenic for 12 weeks on the lipid metabolism were assessed in vivo. We observed that arsenic exposure increased lipogenesis and upregulated DGAT1 expression in rat uroepithelial cells. In vitro studies showed that chronic exposure to arsenic upregulated DGAT1 to store de novo synthesized-fatty acid into triglycerides and lipid droplets. Under arsenic exposure, inhibition of DGAT1 led to excessive fatty acid into the mitochondria for β-oxidation, inducing ferroptosis and suppressing cell proliferation. Additionally, we identified that Jumonji domain-containing 6 (JMJD6) as a key transcriptional regulator of DGAT1 and highlighted the role of JMJD6 in regulating DGAT1 in lipid metabolism remodeling during arsenic-induced malignant phenotype of uroepithelial cells. This study provides new clue for the mechanisms of arsenic carcinogenesis and proposes a reliable reference for mitigating arsenic toxicity.

The repair of alveolar bone defects continues to pose a significant challenge within the field of stomatology. As the primary implant material utilized in clinical treatment, the mechanisms by which calcium phosphate-based materials promote bone formation necessitate further in-depth exploration. Single-cell RNA sequencing was employed to characterize the immune microenvironment surrounding hydroxyapatite (HA)-mediated alveolar bone regeneration, confirming the macrophage-dependent enhancement of regenerative outcomes. Based on this finding, amorphous calcium zinc phosphate (ACZP) nanoparticles were developed as immunomodulatory nanomaterials. ACZP can accelerate bone regeneration via anti-inflammatory phenotype polarization, specifically by inhibiting endoplasmic reticulum-mitochondria coupling, reducing pathological Ca2+ transfer, and shifting macrophage metabolism from glycolysis to oxidative phosphorylation (OXPHOS), thereby enhancing bioenergetics. Our results demonstrated that ACZP can inhibit the IP3R/MCU pathway in macrophages, restoring their anti-inflammatory capabilities and ultimately achieving significant effects in the alveolar bone defects of New Zealand white rabbits. Twelve weeks post-surgery, the defects in the ACZP group were filled with nearly 70 % newly formed bone tissue. This study elucidated the immunomodulatory role of ACZP materials in the dynamic process of alveolar bone healing, providing novel insights and methodologies for the design of materials in the fields of tissue engineering and regenerative medicine.

Epidemiologic research has demonstrated a clear correlation between prolonged exposure to inorganic arsenic and an elevated risk of bladder cancer, but the specific mechanisms are unknown. Calcium ions (Ca2+), as key second messengers, are crucial in cellular physiological and pathological processes. Loss of Ca2+ homeostasis is thought to be an important driver of malignant disease. In this study, C57BL/6 mice were treated with 0, 8, 20 and 50 mg/L NaAsO2 via drinking water during 20 weeks, and human normal bladder epithelial cells (SV-HUC-1) received continuous exposure to 0.5 μM NaAsO2 over 40 weeks. The results revealed that long-term arsenic treatment led to elevated Ca2+ levels in SV-HUC-1 cells and enhanced cell proliferation, stemness, and epithelial-mesenchymal transition (EMT). Our study revealed that store-operated calcium entry (SOCE) was essential in arsenic-induced elevation of Ca2+ levels. STIM1 serves as a critical mediator of arsenic-triggered malignant transformation in urothelial cells by regulating store-operated calcium channels (SOCC). STIM1 undergoes N-linked glycosylation at its N131 site. This post-translational modification is essential for proper STIM1 localization and binding with ORAI1. The evidence, similar to the cellular experiments in vitro, was also observed in animal experiments in vivo. Our research results provide a new mechanism for the role of calcium homeostasis imbalance in arsenic-induced initiation and progression of bladder cancer.

Arsenic (As) is recognized as a potent environmental contaminant associated with bladder carcinogenesis. However, its molecular mechanism remains unclear. Metabolic reprogramming is one of the hallmarks of cancer and is as a central feature of malignancy. Here, we performed the study of cross-talk between the mammalian target of rapamycin complex 1 (mTORC1)/ Hypoxia-inducible factor 1 alpha (HIF-1α) pathway and aerobic glycolysis in promoting the proliferation and migration of bladder epithelial cells treated by arsenic in vivo and in vitro. We demonstrated that arsenite promoted N-methyl-N-nitrosourea (MNU)-induced tumor formation in the bladder of rats and the malignant behavior of human ureteral epithelial (SV-HUC-1) cell. We found that arsenite positively regulated the mTORC1/HIF-1α pathway through glucose transporter protein 1 (GLUT1), which involved in the malignant progression of bladder epithelial cells relying on glycolysis. In addition, pyruvate kinase M2 (PKM2) increased by arsenite reduced the protein expressions of succinate dehydrogenase (SDH) and fumarate hydratase (FH), leading to the accumulation of tumor metabolites of succinate and fumarate. Moreover, heat shock protein (HSP)90, functioning as a chaperone protein, stabilized PKM2 and thereby regulated the proliferation and aerobic glycolysis in arsenite treated SV-HUC-1 cells. Taken together, these results provide new insights into mTORC1/HIF-1α and PKM2 networks as critical molecular targets that contribute to the arsenic-induced malignant progression of bladder epithelial cells.

Biodegradable magnesium-matrix composites (BMMCs) added with bone-like compounds such as hydroxyapatite (HA) have promising orthopedic application potential, but the in vivo results of BMMCs are insufficient, and the difference between in vitro and in vivo are not clarified. In this work, Mg-Zn-Nd-Zr/(10/15/20wt%) HA (Ca10(PO4)6OH2) composites were prepared through friction stirring processing (FSP). It was found that corrosion rate of the composites increased with increase of the HA content, where the corrosion rate from hydrogen evolution of the Mg/10wt% HA was about 0.107 mm/y, showing better corrosion resistance compared with other BMMCs, and the agglomeration of HA powders significantly aggravated the localized corrosion. The ALP specific activity of the MC3T3-E1 cells cultured for 14 days with Mg/10wt% HA (2.12 IU/mg) was higher than that of the matrix (1.85 IU/mg), but there was no difference with the FSP group (2.13 IU/mg). In the early implantation of the rabbit femur, bone volume fraction (BV/TV) of Mg/10wt% HA was 10.69, which was higher than that of the FSP group (6.35). The histological staining showed that the Mg/10wt% HA implant was surrounded by more trabecular bone tissue, exhibiting better osteoinductive regeneration. The Mg-Zn-Nd-Zr/HA composites exhibit higher osteogenic activity in vivo differently from in vitro osteogenic expression.

In recent years, the regulation of the cell microenvironment has opened up new avenues for bone defect repair. Researchers have developed novel biomaterials to influence the behavior of osteoblasts and immune cells by regulating the microenvironment, aiming to achieve efficient bone repair. Mitochondria, as crucial organelles involved in energy conversion, biosynthesis and signal transduction, play a vital role in maintaining bone integrity. Dysfunction of mitochondria can have detrimental effects on the transformation of the immune microenvironment and the differentiation of stem cells, thereby hindering bone tissue regeneration. Consequently, targeted therapy strategies focusing on mitochondria have emerged. This approach offers a wide range of applications and reliable therapeutic effects, thereby providing a new treatment option for complex and refractory bone defect diseases. In recent studies, more biomaterials have been used to restore mitochondrial function and promote positive cell differentiation. The main directions are mitochondrial energy metabolism, mitochondrial biogenesis and mitochondrial quality control. In this review, we investigated the biomaterials used for mitochondria-targeted treatment of bone defect repair in recent years from the perspective of progress and strategies. We also summarized the micro-molecular mechanisms affected by them. Through discussions on energy metabolism, oxidative stress regulation and autophagy regulation, we emphasized the opportunities and challenges faced by mitochondria-targeted biomaterials, providing vital clues for developing a new generation of bone repair materials.

Epidemiological evidence reveals that arsenic increases the risk of chronic kidney disease (CKD) in humans, but its mechanism of action has so far been unclear. Fibrosis is the manifestation of end-stage renal disease. Hypoxia is recognized as a vital event accompanying the progression of renal fibrosis. KM mice were exposed to 0, 20, 40, and 80 mg/L NaAsO2 for 12 weeks. HK-2 cells were treated with 1 mu M NaAsO2 for 4 weeks. The results showed that arsenic increased the expression of hypoxia-inducible factor 1 alpha (HIF-1 alpha) (P < 0.05), which is involved in inorganic arsenic-induced renal fibrosis. The Hippo signaling pathway is the upstream signal of HIF-1 alpha and the kinase cascade of Large tumor suppressor kinase 1 (LATS1) and Yes-associated protein 1 (YAP1) is the heart of the Hippo pathway. Our results showed that protein expressions of LATS1 and phosphorylated YAP1 were decreased, and dephosphorylated YAP1 expression increased in arsenic-treated mouse kidneys and human HK-2 cells (P < 0.05). Our research manifested that arsenic treatment suppressed the Hippo signaling and induced high expression of YAP1 into the nucleus. We also found that YAP1 was involved in arsenic-induced renal fibrosis by forming a complex with HIF-1 alpha and maintaining HIF-1 alpha stability. Our findings indicate that YAP1 is a potential target for molecular-based therapy for arsenic-mediated renal fibrosis.

Bergapten, a furanocoumarin naturally occurring in bergamot essential oil, has been demonstrated to have the potential to alleviate osteoarthritis-related symptoms via its anti-inflammatory activity. Although its systemic bioavailability is limited, its precise mechanisms of action and effects on temporomandibular joint osteoarthritis (TMJOA) and its relationship with the intestinal flora remain unclear. Here, we explored the anti-TMJOA effect of BGT combined with the interleukin-1β-induced inflammatory response of chondrocytes in a monosodium iodoacetate (MIA)-induced TMJOA rat model. It was confirmed that BGT effectively reduced proinflammatory mediators and increased type II collagen, bone volume, and trabecular number of condyles in TMJOA rats. Importantly, the oral administration of BGT altered the intestinal flora of rats by increasing the relative abundances of nine prebiotic species and decreasing the relative abundance of one potential species. In addition, BGT considerably reduced reactive oxygen species (ROS) levels by suppressing glutathione, oxidized glutathione, and superoxide dismutase in the serum and malondialdehyde in urine. These results suggest that BGT exerts a chondroprotective effect, most likely by improving the intestinal flora and reducing ROS production associated with TMJOA in rats. This finding indicates a novel beneficial effect of BGT on the prevention and treatment of TMJOA.