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      The role of animal models in tendon research

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          Abstract

          Tendinopathy is a debilitating musculoskeletal condition which can cause significant pain and lead to complete rupture of the tendon, which often requires surgical repair. Due in part to the large spectrum of tendon pathologies, these disorders continue to be a clinical challenge. Animal models are often used in this field of research as they offer an attractive framework to examine the cascade of processes that occur throughout both tendon pathology and repair. This review discusses the structural, mechanical, and biological changes that occur throughout tendon pathology in animal models, as well as strategies for the improvement of tendon healing.

          Cite this article: Bone Joint Res 2014;3:193–202.

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          Most cited references117

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          Analysis of the tendon cell fate using Scleraxis, a specific marker for tendons and ligaments.

          R Schweitzer, J Chyung, L. Murtaugh … (2001)
          Little is known about the genesis and patterning of tendons and other connective tissues, mostly owing to the absence of early markers. We have found that Scleraxis, a bHLH transcription factor, is a highly specific marker for all the connective tissues that mediate attachment of muscle to bone in chick and mouse, including the limb tendons, and show that early scleraxis expression marks the progenitor cell populations for these tissues. In the early limb bud, the tendon progenitor population is found in the superficial proximomedial mesenchyme. Using the scleraxis gene as a marker we show that these progenitors are induced by ectodermal signals and restricted by bone morphogenetic protein (BMP) signaling within the mesenchyme. Application of Noggin protein antagonizes this endogenous BMP activity and induces ectopic scleraxis expression. However, the presence of excess tendon progenitors does not lead to the production of additional or longer tendons, indicating that additional signals are required for the final formation of a tendon. Finally, we show that the endogenous expression of noggin within the condensing digit cartilage contributes to the induction of distal tendons.
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            Regulation of tendon differentiation by scleraxis distinguishes force-transmitting tendons from muscle-anchoring tendons.

            Lance Price, Sean D. Conner, Clifford J. Tabin … (2007)
            The scleraxis (Scx) gene, encoding a bHLH transcription factor, is expressed in the progenitors and cells of all tendon tissues. To determine Scx function, we produced a mutant null allele. Scx-/- mice were viable, but showed severe tendon defects, which manifested in a drastically limited use of all paws and back muscles and a complete inability to move the tail. Interestingly, although the differentiation of all force-transmitting and intermuscular tendons was disrupted, other categories of tendons, the function of which is mainly to anchor muscles to the skeleton, were less affected and remained functional, enabling the viability of Scx-/- mutants. The force-transmitting tendons of the limbs and tail varied in the severity to which they were affected, ranging from dramatic failure of progenitor differentiation resulting in the loss of segments or complete tendons, to the formation of small and poorly organized tendons. Tendon progenitors appeared normal in Scx-/- embryos and a phenotype resulting from a failure in the condensation of tendon progenitors to give rise to distinct tendons was first detected at embryonic day (E)13.5. In the tendons that persisted in Scx-/- mutants, we found a reduced and less organized tendon matrix and disorganization at the cellular level that led to intermixing of tenocytes and endotenon cells. The phenotype of Scx-/- mutants emphasizes the diversity of tendon tissues and represents the first molecular insight into the important process of tendon differentiation.
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              Tendon healing: repair and regeneration.

              Alexandra R. Buckley, Louis Soslowsky, Pramod Voleti (2011)
              Injury and degeneration of tendon, the soft tissue that mechanically links muscle and bone, can cause substantial pain and loss of function. This review discusses the composition and function of healthy tendon and describes the structural, biological, and mechanical changes initiated during the process of tendon healing. Biochemical pathways activated during repair, experimental injury models, and parallels between tendon healing and tendon development are emphasized, and cutting-edge strategies for the enhancement of tendon healing are discussed.
              Article 0 comments Cited 140 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                M. W. Hast: Role: Research Specialist
                A. Zuskov: Role: Research Specialist
                L. J. Soslowsky: Role: Fairhill Professor of Orthopaedic Surgery URI : http://orthodox.boneandjoint.org.uk/viewprofileinfo.aspx?authorid=1010209
                Journal
                Journal ID (nlm-ta): Bone Joint Res
                Journal ID (iso-abbrev): Bone Joint Res
                Title: Bone & Joint Research
                Publisher: British Editorial Society of Bone and Joint Surgery
                ISSN (Print): 2046-3758
                ISSN (Electronic): 2046-3758
                Publication date Collection: June 2014
                Publication date (Electronic): 01 June 2014
                Volume: 3
                Issue: 6
                Pages: 193-202
                Affiliations
                [1 ]University of Pennsylvania, McKay Orthopaedic Research Laboratory, 424 Stemmler Hall 36th Street and Hamilton Walk, Philadelphia, 19104-6081, USA.
                Author notes
                Correspondence should be sent to Dr L. J. Soslowsky; e-mail: soslowsk@ 123456upenn.edu
                Article
                Publisher ID: 2000281
                DOI: 10.1302/2046-3758.36.2000281
                PMC ID: 4116644
                PubMed ID: 24958818
                SO-VID: f74caa12-6ec7-4db8-b7dd-c62c5416da37
                Copyright © ©2014 The British Editorial Society of Bone & Joint Surgery
                License:

                ©2014 The British Editorial Society of Bone & Joint Surgery. This is an open-access article distributed under the terms of the Creative Commons Attributions licence, which permits unrestricted use, distribution, and reproduction in any medium, but not for commercial gain, provided the original author and source are credited.

                History
                Date received : 10 January 2014
                Date accepted : 24 February 2014
                Funding
                L. J. Soslowsky reports that his institution, the University of Pennsylvania, has received grants from DJO and Amniox, neither of which is related to this article.
                Categories
                Subject: Specialty update: General orthopaedics
                Subject: 10
                Subject: Tendon
                Subject: Tendinopathy
                Subject: Animal Model
                Subject: Literature Review
                Custom metadata
                odf2nlm-version 1.0
                price $2.00
                principal-institution University of Pennsylvania, Philadelphia, United States
                article-type Specialty update: General orthopaedics
                coi-statement None declared

                Keywords: tendon,tendinopathy,animal model,literature review
                Data availability:
                Keywords: tendon, tendinopathy, animal model, literature review

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