Type II Diabetes (T2DM) dramatically impairs the tendon healing response, resulting in decreased collagen organization and mechanics relative to non-diabetic tendons. Despite this burden, there remains a paucity of information regarding the mechanisms that govern impaired healing of diabetic tendons. Mice were placed on either a high fat diet (T2DM) or low fat diet (lean) and underwent flexor tendon transection and repair surgery. Healing was assessed via mechanical testing, histology and changes in gene expression associated with collagen synthesis, matrix remodeling, and macrophage polarization. Obese/diabetic tendons healed with increased scar formation and impaired mechanical properties. Consistent with this, prolonged and excess expression of extracellular matrix (ECM) components were observed in obese/T2DM tendons. Macrophages are involved in both inflammatory and matrix deposition processes during healing. Obese/T2DM tendons healed with increased expression of markers of pro-inflammatory M1 macrophages, and elevated and prolonged expression of M2 macrophages markers that are involved in ECM deposition. Here we demonstrate that tendons from obese/diabetic mice heal with increased scar formation and increased M2 polarization, identifying excess M2 macrophage activity and matrix synthesis as a potential mechanism of the fibrotic healing phenotype observed in T2DM tendons, and as such a potential target to improve tendon healing in T2DM.

Flexor tendon injuries are a common clinical problem, and repairs are frequently complicated by post-operative adhesions forming between the tendon and surrounding soft tissue. Prostaglandin E2 and the EP4 receptor have been implicated in this process following tendon injury; thus, we hypothesized that inhibiting EP4 after tendon injury would attenuate adhesion formation. A model of flexor tendon laceration and repair was utilized in C57BL/6J female mice to evaluate the effects of EP4 inhibition on adhesion formation and matrix deposition during flexor tendon repair. Systemic EP4 antagonist or vehicle control was given by intraperitoneal injection during the late proliferative phase of healing, and outcomes were analyzed for range of motion, biomechanics, histology, and genetic changes. Repairs treated with an EP4 antagonist demonstrated significant decreases in range of motion with increased resistance to gliding within the first three weeks after injury, suggesting greater adhesion formation. Histologic analysis of the repair site revealed a more robust granulation zone in the EP4 antagonist treated repairs, with early polarization for type III collagen by picrosirius red staining, findings consistent with functional outcomes. RT-PCR analysis demonstrated accelerated peaks in F4/80 and type III collagen (Col3a1) expression in the antagonist group, along with decreases in type I collagen (Col1a1). Mmp9 expression was significantly increased after discontinuing the antagonist, consistent with its role in mediating adhesion formation. Mmp2, which contributes to repair site remodeling, increases steadily between 10 and 28 days post-repair in the EP4 antagonist group, consistent with the increased matrix and granulation zones requiring remodeling in these repairs. These findings suggest that systemic EP4 antagonism leads to increased adhesion formation and matrix deposition during flexor tendon healing. Counter to our hypothesis that EP4 antagonism would improve the healing phenotype, these results highlight the complex role of EP4 signaling during tendon repair.

Type II Diabetes (T2DM) dramatically impairs the tendon healing response, resulting in decreased collagen organization and mechanics relative to non-diabetic tendons. Despite this burden, there remains a paucity of information regarding the mechanisms that govern impaired healing of diabetic tendons. Mice were placed on either a high fat diet (T2DM) or low fat diet (lean) and underwent flexor tendon transection and repair surgery. Healing was assessed via mechanical testing, histology and changes in gene expression associated with collagen synthesis, matrix remodeling, and macrophage polarization. Obese/diabetic tendons healed with increased scar formation and impaired mechanical properties. Consistent with this, prolonged and excess expression of extracellular matrix (ECM) components were observed in obese/T2DM tendons. Macrophages are involved in both inflammatory and matrix deposition processes during healing. Obese/T2DM tendons healed with increased expression of markers of pro-inflammatory M1 macrophages, and elevated and prolonged expression of M2 macrophages markers that are involved in ECM deposition. Here we demonstrate that tendons from obese/diabetic mice heal with increased scar formation and increased M2 polarization, identifying excess M2 macrophage activity and matrix synthesis as a potential mechanism of the fibrotic healing phenotype observed in T2DM tendons, and as such a potential target to improve tendon healing in T2DM.

Background The purpose of this narrative review was to survey the literature for common complications following treatment of DDH in children less than 4 years old. Methods The Pubmed database was queried. Search result titles were reviewed to identify papers that were pertinent to the topic. Abstracts for these papers were obtained and read, and a subset of these were selected for review of the complete manuscript. Results 92 manuscripts were reviewed. Residual dysplasia, redislocation, and osteonecrosis are the primary complications of treatment in this age group. In the long term, hips without complications related to DDH treatment tend to do well, although a significant percentage of them will inevitably require joint replacement surgery. Conclusion Although there is excellent potential for a good outcome when DDH is diagnosed and treated under age 4 years, osteonecrosis continues to be a concern with all treatment methods. A subset of patients from this young cohort will continue to have residual dysplasia or recurrent dislocation requiring return to the operating room.

Background After flexor tendon (FT) injury and repair, adhesion formation is a substantial concern as it can result in loss of motion and functional disability. Mmp9 is a gelatinase that contributes to degradation of extracellular matrix and is expressed during FT healing. Mmp9-/- mice have accelerated remodeling of adhesions during FT healing, relative to wild type mice. The purpose of this study was to investigate whether Ro 32-3555, an Mmp9 inhibitor, can improve FT healing by limiting adhesion formation or enhancing remodeling of scar tissue during murine FT healing. Methods Flexor digitorum longus laceration and repair was performed in female C57BL/6J mice. Mice were treated with vehicle or the Mmp9 inhibitor Ro 32-3555 for 8 days. Analysis was performed for digit range of motion and gliding function, biomechanics, gene expression, and Mmp9 activity. Results An Mmp9 activity assay as well as zymography confirmed suppression of Mmp9 activity in mice treated with Ro 32-3555. There was no significant difference in tendon gliding or range of motion between vehicle and Ro 32-3555 treated mice. There was also no difference in tendon biomechanical properties between the two groups. Conclusions Local inhibition of Mmp9 gelatinolytic activity at the FT repair site is insufficient to alter adhesion formation, remodeling of adhesions, and mechanical properties of healing murine flexor tendons.

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Case: Synovial chondromatosis is a rare condition affecting synovial joints. It occurs uncommonly in the shoulder and is rare in the pediatric population. We present a case of a 13-year-old male patient with shoulder pain who was diagnosed with synovial chondromatosis and a posterior labral tear. He was treated with arthroscopic loose body removal, synovectomy, and posterior labral repair and recovered well from the surgery. Four years after the surgery, he developed pain in the same shoulder, but the cause of the pain was not investigated per the patient's decision. Conclusion: Synovial chondromatosis should be considered in pediatric patients presenting with shoulder pain and loss of function with potential for recurrence.