RESUMEN
Diabetic periodontitis (DP) refers to destruction of periodontal tissue and absorption of bone tissue in diabetic patients. Tumor necrosis factor receptorassociated factor (TRAF)interacting protein with forkheadassociated domain (TIFA) as a crucial regulator of inflammation activates the NFκB signaling pathway to regulate cell biological behavior. However, the function and mechanism of TIFA on DP suffer from a lack of research. In the present study, TIFA was upregulated in the periodontal tissue of a DP mouse model. In addition, the expression of TIFA in RAW264.7 cells was induced by high glucose (HG) culture and increased by lipopolysaccharide (LPS) from Porphyromonas gingivalis treatment in a timedependent manner. Knockdown of TIFA significantly reduced the levels of inflammatory cytokines, including TNFα, IL6, IL1ß and monocyte chemoattractant protein1, in HG and LPSinduced RAW264.7 cells. The nuclear translocation of NFκB p65 was induced by HG and LPS and was clearly suppressed by absence of TIFA. The expression of downstream factors Nodlike receptor family pyrin domaincontaining 3 and apoptosisassociated specklike protein was inhibited by silencing TIFA. Moreover, TIFA was increased by receptor activator of NFκB (RANK) ligand (RANKL) in a concentration dependent manner. The expression of cathepsin K, MMP9 and nuclear factor of activated T cells cytoplasmic 1 was downregulated by depletion of TIFA. RANKLinduced osteoclast differentiation was inhibited by silencing of TIFA. Meanwhile, the decrease of TIFA blocked activation of the NFκB pathway in RANKLtreated RAW264.7 cells. In conclusion, TIFA as a promoter regulates the inflammation and osteoclast differentiation via activating the NFκB signaling pathway.
Asunto(s)
Diabetes Mellitus Experimental , Periodontitis , Animales , Humanos , Ratones , Diabetes Mellitus Experimental/genética , Diabetes Mellitus Experimental/metabolismo , Inflamación/metabolismo , Lipopolisacáridos/farmacología , FN-kappa B/metabolismo , Osteoclastos/metabolismo , Periodontitis/genética , Periodontitis/metabolismo , Ligando RANK/genética , Ligando RANK/metabolismo , Receptor Activador del Factor Nuclear kappa-B/metabolismo , Transducción de SeñalRESUMEN
Background: Osteoporosis is a significant barrier to the use of dental implants in the elderly for the treatment of tooth defects. Adipose derived stem cells (ADSCs) have demonstrated extensive potential for tissue repair and regeneration. The present study aimed to investigate the effectiveness of ADSCs engineered to express high levels of osteoprotegerin (OPG) for the treatment of bone loss in implant dentistry caused by estrogen deficiency. Methods: A rat model of osteoporosis was established through double oophorectomy, and the rats were treated by gene modified cells Adv-OPG-ADSCs. The effects of the treatment on maxilla tissue changes were evaluated using HE staining and micro-CT. Additionally, ALP and TRAP staining were used to assess osteoblast and osteoclast alterations. Finally, the changes in related osteoblast and osteoclast indicators were measured by RT-qPCR, Western blot, and ELISA. Results: The successfully generated high-OPG-expressing ADSCs led to increase of cell viability, proliferation, and osteoblast differentiation. Treatment with Adv-OPG-ADSCs significantly ameliorated maxillary morphology, trabecular volume reduction, and bone mineral density decline in the model of estrogen-deficient maxillary implant dentistry. Furthermore, the treatment was beneficial to promoting the generation of osteoblasts and inhibiting the generation of osteoclast. Adv-OPG-ADSCs increased OPG, ALP, OCN, and Runx-2 expressions in the maxilla while suppressing RANKL expression, and also increased the concentration of COL I and PINP, as well as decreased the concentration of CTX-1. Conclusion: Adv-OPG-ADSCs promote the formation of osteoblasts and inhibit the generation of osteoclasts, thereby inhibiting bone absorption, facilitating bone formation, and promoting the repair of maxillary bone after dental implantation in the presence of osteoporosis-related complications, especially in the setting of estrogen deficiency, providing scientific basis for the application of Adv-OPG-ADSCs in the treatment of implant related osteoporosis.
RESUMEN
PURPOSE: The purpose of this study was to evaluate the effect of surgical treatment on displaced and dislocated sagittal fractures of the mandibular condyle (SFMC). PATIENTS AND METHODS: Twenty-four patients with 28 displaced and dislocated SFMCs were distinguished into type M, type C, and type L fractures according the location of the fracture line. The fractured fragment was reduced and fixated with two 0.6-mm 4-hole micro-plates via a preauricular temporal incision. The fragment was extirpated when it was too small to be fixated. The postoperative position and profile of the fragment was examined by orthopantomogram radiograph or computed tomography (CT). The function of the temporal and zygomatic branches of the facial nerve was inspected. The occluding relation was surveyed, the interincisal distance at maximum mouth opening was measured, and the deviation from the midline during mouth opening was recorded. RESULTS: Twenty-three condyles (82%) suffered dislocated fractures with the condylar fragment out of the glenoid fossa. Five condyles (18%) were displaced, but not dislocated. There were 2 (7%) type M, 19 (68%) type C (3 comminuted), and 7 (25%) type L fractures (1 comminuted), respectively. Twenty-one (75%) fractured fragments received free-graft procedures with 2 micro-plates. Four (14%) fragments were reduced and fixated without being dissected free of their attachments. Three (11%) fragments were extirpated. There were no permanent facial never branch injuries. Micro-plate removal was necessary because of postoperative infection and necrosis of the fractured fragment in 1 condylar process. No other patients could be found with obvious postoperative bone resorption. The average postoperative maximum mouth opening and deviation at 6 months were improved significantly. The postoperative occlusion was good in 22 cases. CONCLUSIONS: Access with the preauricular incision, and the dislocated and displaced fragment can be reduced and fixated to its normal position easily. Free-graft procedure is a suitable surgical treatment if the fractured fragment cannot be reduced without dissection free of the pterygoid muscle attachment. Although most fractured fragments in SFMCs have to be dissected free, there are no obvious complications in dislocated and displaced SFMCs after surgical treatment.