Mast Cells Mediate Acute Inflammatory Responses After Glenoid Labral Tears and Can Be Inhibited With Cromolyn in a Rat Model.

Autor:	Co CM; Department of Bioengineering, University of Texas at Arlington, Arlington, Texas, USA.; These authors contributed equally to this article., Vaish B; Department of Bioengineering, University of Texas at Arlington, Arlington, Texas, USA.; These authors contributed equally to this article., Hoang LQ; Department of Bioengineering, University of Texas at Arlington, Arlington, Texas, USA., Nguyen T; Department of Bioengineering, University of Texas at Arlington, Arlington, Texas, USA., Borrelli J Jr; Department of Bioengineering, University of Texas at Arlington, Arlington, Texas, USA., Millett PJ; Department of Orthopedic Surgery, The Steadman Clinic, Vail, Colorado, USA., Tang L; Department of Bioengineering, University of Texas at Arlington, Arlington, Texas, USA.
Jazyk:	angličtina
Zdroj:	The American journal of sports medicine [Am J Sports Med] 2024 Nov; Vol. 52 (13), pp. 3357-3369. Date of Electronic Publication: 2024 Oct 06.
DOI:	10.1177/03635465241278671
Abstrakt:	Background: Injuries to the glenoid labrum have been recognized as a source of joint pain and discomfort, which may be associated with the inflammatory responses that lead to the deterioration of labral tissue. However, it is unclear whether the torn labrum prompts mast cell (MC) activation, resulting in synovial inflammatory responses that lead to labral tissue degeneration. Purpose: To determine the potential influence of activated MC on synovial inflammatory responses and subsequent labral tissue degeneration and shoulder function deterioration in a rat model by monitoring MC behavior and sequential inflammatory responses within the synovial tissue and labral tissue after injury, suture repair, and MC stabilizer administration. Study Design: Controlled laboratory study. Methods: Anteroinferior glenoid labral tears were generated in the right shoulder of rats (n = 20) and repaired using a tunneled suture technique. Synovial tissue inflammatory responses were modulated in some rats with intraperitoneal administration of an MC stabilizer-cromolyn (n = 10). At weeks 1 and 3, MC activation, synovial inflammatory responses, and labral degeneration were histologically evaluated. Simultaneously, gait analysis was performed before and after surgical repair to assess the worsening of the shoulder function after the injury and treatment. Results: Resident MC degranulation after labral injury (50.48% ± 8.23% activated at week 1) contributed to the initiation of synovial tissue inflammatory cell recruitment, inflammatory product release, matrix metalloproteinase-13, and subsequent labral tissue extracellular matrix degeneration. The administration of cromolyn, an MC stabilizer, was found to significantly diminish injury-mediated inflammatory responses (inflammatory cell infiltration and subsequent proinflammatory product secretion) and improve shoulder functional recovery. Conclusion: MC activation is responsible for labral tear-associated synovial inflammation and labral degeneration. The administration of cromolyn can significantly diminish the cascade of inflammatory reactions after labral injury. Clinical Relevance: Our findings support the concept that MC stabilizers may be used as a complementary therapeutic option in the treatment and repair of labral tears. Competing Interests: One or more of the authors has declared the following potential conflict of interest or source of funding: This work was supported by the National Institutes of Health RO1 (AR081979). L.T. has a potential financial interest in Progenitec Inc, a wound diagnostic device company. A management plan has been created to preserve objectivity in the research in accordance with the University of Texas at Arlington's policy. P.J.M. has received consulting fees, intellectual property royalties, and research support from Arthrex Inc; and holds stocks in VuMedi. P.J.M. is an employee of the Steadman Philippon Research Institute (SPRI). The SPRI exercises special care in identifying any financial interests or relationships related to research conducted here. During the past calendar year, the SPRI has received grant funding or in-kind donations from Arthrex, Canon, DJO, Icarus Medical, Medtronic, Ossur, Smith & Nephew, SubioMed, Stryker, and Wright Medical. J.B. has received consulting fees from Amgen Inc and hospitality payments from Zimmer Biomet. AOSSM checks author disclosures against the Open Payments Database (OPD). AOSSM has not conducted an independent investigation on the OPD and disclaims any liability or responsibility relating thereto. The authors acknowledge the support from the National Institutes of Health (AR081979). The content is the authors’ sole responsibility and does not necessarily represent the official views of the National Institutes of Health.
Databáze:	MEDLINE
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