Interaction behaviors of sulfamethoxazole and microplastics in marine condition: Focusing on the synergistic effects of salinity and temperature.

Microplastics and antibiotics are two common pollutants in the ocean. However, due to changes of salinity and temperature in the ocean, their interaction are significantly different from that of fresh water, and the mechanism remains unclear. Here, the interactions of sulfamethoxazole (SMZ) and microplastics were studied at different temperatures and salinities. The saturation adsorption capacity of SMZ in polypropylene (PP), polyethylene (PE), styrene (PS), polyvinyl chloride (PVC), and synthetic resins (ABS) were highest at the temperature of 20 °C, with 0.118 ± 0.002 mg·g-1, 0.106 ± 0.004 mg·g-1, 0.083 ± 0.002 mg·g-1, 0.062 ± 0.007 mg·g-1 and 0.056 ± 0.003 mg·g-1, respectively. The effect of temperature reduction is more significant than temperature rise. The intraparticle diffusion model is appropriate to PP, when film diffusion model suited for PS. The salinity has a more significant effect than temperature on different microplastics, due to the electrostatic adsorption and iron exchange. With the increase in salinity from 0.05% to 3.5%, the adsorption capacity of microplastics on SMZ fell by 53.3 ± 5%, and there was no discernible difference of various microplastics. The hydrogen bond and π-π conjugation of microplastics play an important role in the adsorption of SMZ. These findings further deepen the understanding of the interaction between microplastics and antibiotics in the marine environment.

Combined degenerative and regenerative remodeling responses of the mandibular condyle to experimentally induced disordered occlusion.

INTRODUCTION: The purposes of this research were to investigate the long-term responses of mandibular condylar cartilage to experimentally induced disordered occlusion and to evaluate changes in the expression of the SDF-1/CXCR4 axis. METHODS: Experimentally induced disordered occlusions were created in 8-week-old female Sprague-Dawley rats by orthodontic methods. After 24 weeks, remodeling of the mandibular condylar cartilage was assessed by hematoxylin and eosin staining. Protein and mRNA expression of SDF-1, CXCR4, MMP9, IL6, OPG, and RANKL were investigated by means of immunohistochemical staining and real-time polymerase chain reaction. RESULTS: Obvious cartilage degenerative remodeling responses were observed; they appeared as uneven distributions of cellular disposition, loss of cartilage surface integrity, and cell-free areas. Regenerative responses presenting as thickening of the whole and the calcified cartilage layers in the experimental group were also observed. Compared with the age-matched controls, the protein and mRNA levels of SDF-1, CXCR4, MMP9, IL6, and OPG, but not RANKL, were increased in the experimental group (all, P <0.05). In addition, the mRNA level of RANKL/OPG showed a decreasing trend in the experimental group compared with the age-matched controls (P = 0.052). CONCLUSIONS: This study demonstrated that long-term experimentally induced disordered occlusion leads to a combined response in degeneration and regeneration of mandibular cartilage, accompanied by active interaction of the SDF-1/CXCR4 axis and local upregulation of MMP9, IL6, and OPG.

Biomechanically stimulated chondrocytes promote osteoclastic bone resorption in the mandibular condyle.

OBJECTIVE: Chondrocyte signaling is important in osteoclastic bone resorption in mice tibiae. The present study aimed to test whether biomechanically stimulated chondrocytes promote osteoclastic bone resorption in the mandibular condyle. METHODS: Primary chondrocytes isolated from rat condylar cartilage were stimulated by fluid flow shear stress (FSS) for 30, 60, 120 min at intensities of 10, 20, or 30 dynes/cm2. The levels of pro-osteoclastic factors and pro-osteoclastic function of FSS-stimulated chondrocytes were tested. Abnormal molar occlusion was established in rats, and the relationship between cartilage degeneration and osteoclastogenesis in the subchondral bone of the mandibular condyle, and the expression of pro-osteoclastic factors in condylar cartilage, were evaluated. RESULTS: The mRNA and protein levels of SDF-1 and TGFß-1 increased significantly in all FSS-treated groups; the levels of RANKL and RANKL:OPG increased in all intensities and in 60 and 120 min of FSS; and those of Wnt5 A increased in all time-points and in 20 and 30 dynes/cm2 of FSS-treated groups (all compared with their levels the controls; P < 0.05). The percent area of degenerative cartilage changes correlated positively with osteoclast number and osteoclast surface/bone surface in the mandibular condyles of abnormal occlusion rats (P < 0.05). Abnormal occlusion increased the immune-positive area and the mRNA expression levels of Sdf1, Tgfb1, Rankl, Wnt5a and the RANKL:OPG ratio in rat condylar cartilage compared with those in the controls (all P < 0.05). CONCLUSION: Chondrocytes under mechanical stimulation could express higher levels of pro-osteoclastic factors and induced condylar subchondral bone resorption by promoting osteoclastogenesis.

Response of mandibular condyles of juvenile and adult rats to abnormal occlusion and subsequent exemption.

OBJECTIVE: The adaptation capacities of the mandibular condyle in response to mechanical stimuli might be different between juveniles and adults, but has not been compared. This study aimed to investigate whether abnormal molar occlusion and subsequent molar extraction could lead to different remodeling responses in the mandibular condyles of juvenile and adult rats. METHODS: Abnormal molar occlusion (AMO) was established in the 5- and 16-wk old rats by moving their maxillary left and mandibular right third molars distally. AMO was removed in the molar extraction group at 4 weeks but remained in the AMO group. All rats were sacrificed at 8 weeks. Micro-computed tomography, histomorphology, immunohistochemistry and real-time PCR were adopted to evaluate the remodeling of condylar subchondral bone. RESULTS: Condylar subchondral bone loss and increased osteoclastic activities were observed in both juvenile and adult AMO groups, while increased osteoblastic activities were only seen in the juvenile AMO group. Decreased bone mineral density, bone volume fraction and trabecular thickness, but increased trabecular separation, number and surface of osteoclasts and mRNA levels of TRAP, cathepsin-K, RANKL in the juvenile AMO group were all reversed after molar extraction (all P<0.05). However, these parameters showed no difference between adult AMO and extraction groups (all P>0.05). CONCLUSIONS: Abnormal molar occlusion led to degenerative remodeling in the mandibular condyles of both juvenile and adult rats, while exemption of abnormal occlusion caused significant rescue of the degenerative changes only in the juvenile rats.

Osteochondral angiogenesis in rat mandibular condyles with osteoarthritis-like changes.

OBJECTIVE: To investigate angiogenesis at the osteochondral junction and changes in expression of pro- and anti-angiogenic factors in rat mandibular condyles with osteoarthritis-like changes. METHODS: In order to evoke osteoarthritis-like lesions in mandibular condyles, disordered occlusion was created experimentally in rats. Osteochondral vascularity was assessed histologically at 20 and 24 weeks. Protein and mRNA levels of pro-angiogenic factors including vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF) and matrix metalloproteases 9 (MMP9), and anti-angiogenic factor chondromodulin-I (CHM-I) were investigated by means of immunohistochemical staining and real-time PCR. RESULTS: Osteochondral angiogenesis was demonstrated as increased numbers of vascular channels terminating in the calcified cartilage and non-calcified cartilage in 20- and 24-week experimental groups compared with controls (all P<0.05). In the experimental groups, VEGF, CTGF and MMP9 were highly expressed in the tissues adjacent to the osteochondral junction. However, CHM-I was more expressed in the superior but not deep hypertrophic chondrocytes. Compared to their age-matched controls, the protein levels of VEGF and CTGF were higher in 20-week experimental group, and the protein and mRNA levels of CTGF, MMP-9, and CHM-I increased in the 24-week experimental group (all P<0.05). CONCLUSION: In the present rat model, osteochondral angiogenesis was observed in mandibular condyles with osteoarthritis-like changes, accompanied with local upregulation of VEGF, CTGF and MMP9. Although the increase in CHM-I may moderate pro-angiogenic factors effects in the superior cartilage, the deficiency of deep hypertrophic chondrocytes to express CHM-I may permit vascular invasion into condylar cartilage.