Abstract
The origin of cells that contribute to tendon healing, specifically extrinsic epitenon/paratenon cells vs. internal tendon fibroblasts, is still debated. The purpose of this study is to determine the location and phenotype of cells that contribute to healing of a central patellar tendon defect injury in the mouse. Normal adult patellar tendon consists of scleraxis-expressing (Scx) tendon fibroblasts situated among aligned collagen fibrils. The tendon body is surrounded by paratenon, which consists of a thin layer of cells that do not express Scx and collagen fibers oriented circumferentially around the tendon. At 3 days following injury, the paratenon thickens as cells within the paratenon proliferate and begin producing tenascin-C and fibromodulin. These cells migrate toward the defect site and express scleraxis and smooth muscle actin alpha by day 7. The thickened paratenon tissue eventually bridges the tendon defect by day 14. Similarly, cells within the periphery of the adjacent tendon struts express these markers and become disorganized. Cells within the defect region show increased expression of fibrillar collagens (Col1a1 and Col3a1) but decreased expression of tenogenic transcription factors (scleraxis and mohawk homeobox) and collagen assembly genes (fibromodulin and decorin). By contrast, early growth response 1 and 2 are upregulated in these tissues along with tenascin-C. These results suggest that paratenon cells, which normally do not express Scx, respond to injury by turning on Scx and assembling matrix to bridge the defect. Future studies are needed to determine the signaling pathways that drive these cells and whether they are capable of producing a functional tendon matrix. Understanding this process may guide tissue engineering strategies in the future by stimulating these cells to improve tendon repair.
Highlights
Tendon injuries remain a significant socioeconomic problem that requires innovative treatment strategies for repair [1]
Expression of Tenogenic Markers in Normal Tendon The patellar tendon in cross section consists of ScxGFP+ cells throughout the tendon and retinaculum on the medial and lateral sides (Figs. 1–4A)
The objective of this study was to determine 1) the origin and 2) phenotype of cells within the paratenon and adjacent tendon struts that contribute to the repair process following a central patellar tendon defect injury in ScxGFP mice
Summary
Tendon injuries remain a significant socioeconomic problem that requires innovative treatment strategies for repair [1]. Investigators have tried to isolate tendon-specific progenitors for use in tissue-engineered repair [2,3]. Researchers still debate the location of cells within or around tendon that contribute to healing and whether these cells are tissue-resident progenitors [4]. Recent developmental work has provided insight into molecular markers and signaling pathways that influence tendon differentiation [5,6,7]. This current study will utilize these new tools to begin to identify the cells that contribute to the tendon healing process by determining 1) their origin and 2) their expression of tenogenic markers
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