Abstract
ObjectivesTo (i) use a mandibular advancement appliance in rats to investigate the role of the stromal cell-derived factor/CXC receptor 4 (SDF-1/CXCR4) signaling pathway in temporomandibular joint osteoarthritis (TMJ OA) induced by overloaded functional orthopedics (OFO) and (ii) provide a cellular and molecular basis for efficacious treatment of skeletal class-II malocclusion and avoidance of TMJ OA.MethodMale Sprague-Dawley rats (6 weeks) were divided randomly into control + normal saline (NS), EXP + ADM3100 (SDF-1 antagonist), EXP + NS, and control + ADM3100 groups. Changes in articular cartilage and subchondral bone after TMJ OA in these four groups were observed by hematoxylin and eosin (H&E), immunofluorescence double staining (IDS), Safranin-O staining, immunohistochemical (IHC) staining, real-time polymerase chain reaction, and micro-computed tomography at 2, 4, and 8 weeks.ResultsOFO led to increased expression of SDF-1, CXCR4, and matrix metalloproteinase (MMP) 13 and decreased expression of collagen II. The thickness of the hypertrophic cartilage layer was reduced at 4 weeks in the EXP + NS group, and damage to subchondral bone was observed at 2 weeks. Using ADM3100 to inhibit SDF-1 signaling could attenuate expression of MMP13, cartilage damage, and osteoblast differentiation. IDS showed that the areas of expression of SDF-1 and OSX in subchondral bone overlapped.ConclusionsOverloaded functional orthopedics (OFO) induced TMJ OA. The destruction of subchondral bone in TMJ OA caused by OFO occurred before damage to cartilage. SDF-1/CXCR4 may induce the osteogenic differentiation and cause cartilage degradation in TMJ OA caused by OFO.
Highlights
Class-II malocclusion is characterized by a convex facial profile, protrusive and everted lips, and a deep mentolabial fold
We found that the continuous force applied by overloaded functional orthopedics (OFO) increased mRNA and protein expression of Stromal cell-derived factor-1 (SDF-1) and CXC receptor 4 (CXCR4), caused cartilage degradation, and reduced expression of collagen II in the experimental groups compared with agematched controls
We found that OFO induced temporomandibular joint (TMJ) temporomandibular joint osteoarthritis (OA) in rats
Summary
Class-II malocclusion is characterized by a convex facial profile, protrusive and everted lips, and a deep mentolabial fold. Functional therapy is an effective strategy to coordinate the relationship between maxillary and mandibular structures in growing patients, which is based on adaptive remodeling of the temporomandibular joint (TMJ) [2]. During treatment based on functional orthopedics, the TMJ maintains a balance between anabolism and catabolism with regard to adaptive remodeling [6]. Once biomechanical stimuli exceed the capacity for adaptive remolding of the TMJ, production of inflammatory factors and matrix metalloproteinases (MPPs) will increase, and symptoms of a temporomandibular disorder will be detected: this is called “temporomandibular joint osteoarthritis” (TMJ OA) induced by overloaded functional orthopedics (OFO) [7]. Exploring the mechanism of TMJ OA induced by OFO could provide new approaches for clinical treatment of class-II malocclusions
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