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Bajaj, Anubha. "The Tendinous Impaction- Fibroma of Tendon Sheath." Journal of Clinical Research and Reports 5, no. 1 (July 28, 2020): 01–04. http://dx.doi.org/10.31579/2690-1919/104.
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Preface Fibroma of tendon sheath (FTS) was initially scripted by Geschickter et al in 1949. Subsequently, Chung and Enzinger elaborated upon cogent clinical and pathological manifestations of the neoplasm. Fibroma of tendon sheath is denominated as a benign, fibroblastic, nodular neoplasm which emerges from synovium of tendon sheath. As fibroma of tendon sheath characteristically originates from adherent tendons and tendon sheaths, it predominantly incriminates small joints of upper limb as fingers, hands and wrists. Infrequently, the toe, foot, ankle, leg, knee, shoulder, elbow, forearm, chest, back and temporomandibular joints are implicated.
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Belmahi, A., N.-E. Gharib, and S. El Mazouz. "La greffe tendineuse protégée en zone 2 ou le piège à fibroblastes." Chirurgie de la Main 23, no. 3 (June 2004): 142–48. http://dx.doi.org/10.1016/j.main.2004.04.007.
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Kesyan, G. A., G. N. Berchenko, T. G. Nakhapetyan, N. S. Gavryushenko, R. Z. Uraxgil’deev, D. S. Mikelaishvili, I. G. Arsen’ev, D. R. Muradyan, and I. M. Dan. "Experimental Morphologic and Clinical Substantiation of Autothrombocytic Growth Factors in Complex Treatment of Achilles Tendon Rupture." N.N. Priorov Journal of Traumatology and Orthopedics 19, no. 4 (December 15, 2012): 32–37. http://dx.doi.org/10.17816/vto20120432-37.
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Study of the influence of autothrombocytic growth factors upon the injured tendinous tissue was performed. Experimental results (60 Chinchilla rabbits, 3—5 kg) showed that administration of autologous platelet-rich plasma (PRP) into Achilles tendon (AT) injury zone promoted activiza- tion of reparative processes with diminution of inflammatory manifestations; increase in angio- genesis, proliferative and synthetic fibroblasts activity, fibrillogenesis processes; earlier tendon healing. Clinical study included 57 patients (33—68years) with acute (8—48 hours) and old (1—12 months) AT ruptures. After AT surgical reconstruction(Cuneo tendon sutures in acute AC ruptures and Chernavsiautoplasty in the old ones) PRP was additionally administrated to 30 patients from the main group. Treatment results were evaluated by J. Leppilahti and AOFAS scales in 4 months after surgical intervention. In no one patient from the main group AT reruptures were recorded while in control groupreruptures were recorded in 26% of patients.
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Heinemeier, Katja, Henning Langberg, Jens L. Olesen, and Michael Kjaer. "Role of TGF-β1 in relation to exercise-induced type I collagen synthesis in human tendinous tissue." Journal of Applied Physiology 95, no. 6 (December 2003): 2390–97. http://dx.doi.org/10.1152/japplphysiol.00403.2003.
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Mechanical loading of tissue is known to influence local collagen synthesis, and microdialysis studies indicate that mechanical loading of human tendon during exercise elevates tendinous type I collagen production. Transforming growth factor-β1 (TGF-β1), a potent stimulator of type I collagen synthesis, is released from cultured tendon fibroblasts in response to mechanical loading. Thus TGF-β1 could link mechanical loading and collagen synthesis in tendon tissue in vivo. Tissue levels of TGF-β1 and type I collagen metabolism markers [procollagen I COOH-terminal propeptide (PICP) and COOH-terminal telopeptide of type I collagen (ICTP)] were measured by microdialysis in peritendinous tissue of the Achilles' tendon in six male volunteers before and after treadmill running (1 h, 12 km/h, 3% uphill). In addition, blood levels of TGF-β1, PICP, and ICTP were obtained. PICP levels increased 68 h after exercise ( P < 0.05). Dialysate levels of TGF-β1 changed from 303 ± 46 pg/ml (at rest) to 423 ± 86 pg/ml 3 h postexercise. This change was nonsignificant, but the decay of tissue TGF-β1 after catheter insertion was markedly delayed by exercise compared with the decay seen in resting subjects. Plasma concentrations of TGF-β1 rose 30% in response to exercise ( P < 0.05 vs. pre). Our observations indicate an increased local production of type I collagen in human peritendinous tissue in response to uphill running. Although not conclusive, changes in circulating and local TGF-β1, in response to exercise, suggest a role for TGF-β1 in mechanical regulation of local collagen type I synthesis in tendon-related connective tissue in vivo.
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Yamamoto, N., K. Ohno, K. Hayashi, H. Kuriyama, K. Yasuda, and K. Kaneda. "Effects of Stress Shielding on the Mechanical Properties of Rabbit Patellar Tendon." Journal of Biomechanical Engineering 115, no. 1 (February 1, 1993): 23–28. http://dx.doi.org/10.1115/1.2895466.
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Mechanical properties of the stress-shielded patellar tendon were studied in the rabbit knee. Stress shielding was accomplished by stretching a stainless-steel wire installed between the patella and tibial tubercle and thus, releasing the tension in the patellar tendon completely. Tensile tests were carried out on the specimens obtained from the patellar tendons which were exposed to the stress shielding for 1 to 6 weeks. The stress shielding changed the mechanical properties of the patellar tendon significantly: it decreased the tangent modulus and tensile strength to 9 percent of the control values after 3 weeks. There was a 131 percent increase in the cross-sectional area and a 15 percent decrease in the tendinous length. Remarkable changes were also observed in the structural properties: for example, the maximum load of the bone-tendon complex decreased to 20 percent of the control value after 3 weeks. Histological studies showed that the stress shielding increased the number of fibroblasts and decreased the longitudinally aligned collagen bundles. These results imply that if no stress is applied to the autograft in the case of augmentative reconstruction of the knee ligament, the graft strength decreases remarkably.
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Tavares Junior, Wilson Campos, Eduardo Paulino, Maria Angélica Baron Magalhaes, Ana Clara Guimarães Gabrich Fonseca, João Bernardo Sancio Rocha Rodrigues, and Vivian Resende. "MAGNETIC RESONANCE IMAGING PERFUSION TECHNIQUE IN THE EVALUATION OF ACHILLES TENDON INJURY IN RABBITS." Acta Ortopédica Brasileira 27, no. 1 (February 2019): 12–15. http://dx.doi.org/10.1590/1413-785220192701132230.
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ABSTRACT Objective: This study aimed to evaluate the dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) in the experimental model of Achilles tendon injury. Methods: Twelve white male adults New Zealand rabbits were divided into two groups, a group with resection of the central portion of the Achilles tendon (n = 8) and a control group (n = 4). Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) was performed 4 weeks after the surgical procedure, followed by histological analysis of the tendons. Results: The main finding of this study was the difference (p < 0.001) in peak contrast enhancement on DCE-MRI, which demonstrated that the operated group had greater contrast uptake. The operated tendons showed histological disruption of their architecture, and cluttered appearance of tendinous fibers, with vascular and fibroblast proliferations. Conclusion: DCE-MRI is a technique with a potential to demonstrate changes in the vascularity pattern of the Achilles tendon before and after operation. DCE-MRI has a potential to be used in studies of tendinosis diagnosis and surgical follow-up. Level of evidence II, Experimental Study.
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Sano, H., R. Forough, J. A. Maier, J. P. Case, A. Jackson, K. Engleka, T. Maciag, and R. L. Wilder. "Detection of high levels of heparin binding growth factor-1 (acidic fibroblast growth factor) in inflammatory arthritic joints." Journal of Cell Biology 110, no. 4 (April 1, 1990): 1417–26. http://dx.doi.org/10.1083/jcb.110.4.1417.
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The synovium from patients with rheumatoid arthritis (RA) and LEW/N rats with streptococcal cell wall (SCW) arthritis, an experimental model resembling RA, is characterized by massive proliferation of synovial connective tissues and invasive destruction of periarticular bone and cartilage. Since heparin binding growth factor (HBGF)-1, the precursor of acidic fibroblast growth factor (FGF), is a potent angiogenic polypeptide and mitogen for mesenchymal cells, we sought evidence that it was involved in the synovial pathology of RA and SCW arthritis. HBGF-1 mRNA was detected in RA synovium using the polymerase chain reaction technique, and its product was immunolocalized intracellularly in both RA and osteoarthritis (OA) synovium. HBGF-1 staining was more extensive and intense in synovium of RA patients than OA and correlated with the extent and intensity of synovial mononuclear cell infiltration. HBGF-1 staining also correlated with c-Fos protein staining. In SCW arthritis, HBGF-1 immunostaining was noted in bone marrow, bone, cartilage, synovium, ligamentous and tendinous structures, as well as various dermal structures and developed early in both T-cell competent and incompetent rats. Persistent high level immunostaining of HBGF-1 was only noted in T-cell competent rats like the disease process in general. These observations implicate HBGF-1 in a multitude of biological functions in inflammatory joint diseases.
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Olesen, Jens L., Katja M. Heinemeier, Fadia Haddad, Henning Langberg, Allan Flyvbjerg, Michael Kjær, and Kenneth M. Baldwin. "Expression of insulin-like growth factor I, insulin-like growth factor binding proteins, and collagen mRNA in mechanically loaded plantaris tendon." Journal of Applied Physiology 101, no. 1 (July 2006): 183–88. http://dx.doi.org/10.1152/japplphysiol.00636.2005.
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Insulin-like growth factor I (IGF-I) is known to exert an anabolic effect on tendon fibroblast production of collagen. IGF-I's regulation is complex and involves six different IGF binding proteins (IGFBPs). Of these, IGFBP-4 and -5 could potentially influence the effect of IGF-I in the tendon because they both are produced in fibroblast; however, the response of IGFBP-4 and -5 to mechanical loading and their role in IGF-I regulation in tendinous tissue are unknown. A splice variant of IGF-I, mechano-growth factor (MGF) is upregulated and known to be important for adaptation in loaded muscle. However, it is not known whether MGF is expressed and upregulated in mechanically loaded tendon. This study examined the effect of mechanical load on tendon collagen mRNA in relation to changes in the IGF-I systems mRNA expression. Data were collected at 2, 4, 8 and 16 days after surgical removal of synergistic muscle to the plantaris muscle of the rat, thus increasing the load to plantaris muscle and tendon. Nearly a doubling of the tendon mass was observed after 16 days of loading. A rapid rise in tendon procollagen III mRNA was seen after 2 days whereas the increase in procollagen I mRNA was significant from day 8. MGF was expressed and upregulated in loaded tendon tissue with a faster response than IGF-I, which was increased from day 8. Finally, IGFBP-4 mRNA was increased with a time pattern similar to procollagen III, whereas IGFBP-5 decreased at day 8. In conclusion, loading of tendon tissue results in an upregulation of IGF-I, IGFBP-4, and procollagen and is associated with an increase in tendon mass. Also, MGF is expressed with an early upregulation in loaded tendon tissue. We suggest that the IGF-I system could be involved in collagen synthesis in tendon in response to mechanical loading.
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Bratu, A. M., I. A. Sălcianu, A. I. Nicula, C. Zaharia, and A. N. Marinescu. "Giant Cell Tumours of the Tendon Sheath – Particular MRI Aspect." Romanian Journal of Orthopaedic Surgery and Traumatology 1, Supplement (June 1, 2018): 44. http://dx.doi.org/10.2478/rojost-2018-0055.
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Abstract Giant cell tumor of soft tissue (GCTST) is usually of synovial origin. It affects synovial membrane, serous bursae, and tendinous tunnels. The most common localizations are in the hands and forearms. Anatomopathological, GCTST is considered as being composed of a cellular fibroblastic stroma in which the tumor cells are distributed. This type of tumor is composed of a mononuclear complex and osteoclast-like giant multinucleated cells, similar to those found in the giant cell tumor at the bone level. Histologically, some authors consider that GCTST is a strictly benign tumor, consisting of welldefined multinucleated histiocytes admixed with eosinophils, lymphocytes and scattered spindleshaped cells, or hemosiderin deposits in its structure, and tumor cells do not have mitosis or atypia. Other authors consider that GCTST is a type of low-grade sarcoma; this entity was named “malignant fibrous histiocytoma, giant cell type” due to the histological similarity with malignant fibrous histiocytoma. The case of a female patient, suspected of giant cell tumor of the brachioradialis tendon sheath was presented. The MRI aspect of this tumor is not the typical one. The MRI examination consisted of a series of sequences, with T1 and T2 weighted images, fat suppression sequence, performed in all three planes, axial, sagittal, and coronal. Also, the examination was performed native, after the administration of intravenous contrast substance, when the 3D multiplanar sequences were performed. The final diagnosis was the post-operative anatomopathological examination, which confirmed that it was a giant cell tumor. We present this case for its less frequent localization - forearm, and the interest it might have in surgical treatment.
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Zamboulis, D. E., F. S. S. Ali, and C. T. Thorpe. "ESTABLISHING NOVEL MARKERS OF TENDON CELL POPULATIONS." Orthopaedic Proceedings 106-B, SUPP_1 (January 2, 2024): 76. http://dx.doi.org/10.1302/1358-992x.2024.1.076.
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Energy storing tendons such as the human Achilles and equine superficial digital flexor tendon (SDFT) are prone to age-related injury. Tendons have poor healing capacity and a lack of effective treatments can lead to ongoing pain, reduced function and re-injury. It is therefore important to identify the mechanisms underpinning age-related tendinous changes in order to develop more effective treatments. Our recent single cell sequencing data has shown that tendon cell populations have extensive heterogeneity and cells housed in the tendon interfascicular matrix (IFM) are preferentially affected by ageing. There is, however, a lack of established surface markers for cell populations in tendon, limiting the capacity to isolate distinct cell populations and study their contribution to age-related tendon degeneration. Here, we investigate the presence of the cell surface proteins MET proto-oncogene (MET), integrin subunit alpha 10 (ITGA10), fibroblast activation protein alpha (FAP) and platelet derived growth factor receptor alpha (PDGFRA) in the equine SDFT cell populations and their co-localisation with known markers.Using Western blot we validated the specificity of selected antibodies in equine tissue before performing immunohistochemistry to establish the location of the respective proteins in the SDFT. We subsequently used double labelling immunofluorescence with the established mural cell marker desmin (DES) to distinguish between tenocyte and mural cell populations.In situ, MET, ITGA10, and FAP presence was found in cells throughout the tendon whereas PDGFRA was present in cells within the IFM. Double labelling immunofluorescence with the mural cell marker DES showed lack of co-localisation between PDGFRA and DES suggesting PDGFRA is labelling an IFM cell population distinct from those associated with blood vessels.PDGFRA is a promising target for the specific cell sorting of IFM-localised tenocytes, enabling their isolation and subsequent characterisation.Acknowledgments: The authors acknowledge the Biotechnology and Biological Sciences Research Council (BB/W007282/1) for funding this work.
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Xiao, Han, Yang Chen, Muzhi Li, Qiang Shi, Yan Xu, Jianzhong Hu, Xing Li, Can Chen, and Hongbin Lu. "Cell-Free Book-Shaped Decellularized Tendon Matrix Graft Capable of Controlled Release of BMP-12 to Improve Tendon Healing in a Rat Model." American Journal of Sports Medicine 49, no. 5 (March 5, 2021): 1333–47. http://dx.doi.org/10.1177/0363546521994555.
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Background: Achilles tendon (AT) defects often occur in traumatic and chronic injuries. Currently, no graft can satisfactorily regenerate parallel tendinous tissue at the defect site to completely restore AT function. Purpose: To develop a cell-free functional graft by tethering bone morphogenetic protein 12 (BMP-12) on a book-shaped decellularized tendon matrix (BDTM) and to determine whether this graft is more beneficial for AT defect healing than an autograft. Study Design: Controlled laboratory study. Methods: Canine patellar tendon was sectioned into a book shape and decellularized to fabricate a BDTM. The collagen-binding domain (CBD) was fused into the N-terminus of BMP-12 to synthesize a recombinant BMP-12 (CBD-BMP-12), which was tethered to the BDTM to prepare a cell-free functional graft (CBD-BMP-12/BDTM). After its tensile resistance, tenogenic inducibility, and BMP-12 release dynamics were evaluated, the efficacy of the graft for tendon regeneration was determined in a rat model. A total of 140 mature male Sprague-Dawley rats underwent AT tenotomy. The defect was reconstructed with reversed AT (autograft group), native BMP-12 tethered to an intact decellularized tendon matrix (IDTM; NAT-BMP-12/IDTM group), native BMP-12 tethered to a BDTM (NAT-BMP-12/BDTM group), CBD-BMP-12 tethered on an IDTM (CBD-BMP-12/IDTM group), and CBD-BMP-12 tethered on a BDTM (CBD-BMP-12/BDTM group). The rats were sacrificed 4 or 8 weeks after surgery to harvest AT specimens. Six specimens from each group at each time point were used for histological evaluation; the remaining 8 specimens were used for biomechanical testing. Results: In vitro CBD-BMP-12/BDTM was noncytotoxic, showed high biomimetics with native tendons, was suitable for cell adhesion and growth, and had superior tenogenic inducibility. In vivo the defective AT in the CBD-BMP-12/BDTM group regenerated more naturally than in the other groups, as indicated by more spindle-shaped fibroblasts embedded in a matrix of parallel fibers. The biomechanical properties of the regenerated AT in the CBD-BMP-12/BDTM group also increased more significantly than in the other groups. Conclusion: CBD-BMP-12/BDTM is more beneficial than autograft for healing AT defects in a rat model. Clinical Relevance: The findings of this study demonstrate that CBD-BMP-12/BDTM can serve as a practical graft for reconstructing AT defects.
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Ren, Ye, Rou Wan, Gongyin Zhao, Tomoyuki Kuroiwa, Steven L. Moran, Anne Gingery, and Chunfeng Zhao. "Gene Expression of Postn and FGF7 in Canine Chordae Tendineae and Their Effects on Flexor Tenocyte Biology." Journal of Orthopaedic Research, November 22, 2023. http://dx.doi.org/10.1002/jor.25745.
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Abstract Chordae tendineae, referred to as heart tendinous cords, act as tendons connecting the papillary muscles to the valves in the heart. Their role is analogous to tendons in the musculoskeletal system. Despite being exposed to millions of cyclic tensile stretches over a human's lifetime, chordae tendineae rarely suffer from overuse injuries. On the other hand, musculoskeletal tendinopathy is very common and remains challenging in clinical treatment. The objective of this study was to investigate the mechanism behind the remarkable durability and resistance to overuse injuries of chordae tendineae, as well as to explore their effects on flexor tenocyte biology. The mRNA expression profiles of chordae tendineae were analyzed using RNA sequencing and verified by quantitative reverse transcription polymerase chain reaction (qRT‐PCR) and immunohistochemistry (IHC). Interestingly, we found that periostin (Postn) and fibroblast growth factor 7 (FGF7) were expressed at significantly higher levels in chordae tendineae, compared to flexor tendons. We further treated flexor tenocytes in vitro with periostin and FGF7 to examine their effects on the proliferation, migration, apoptosis, and tendon‐related gene expression of flexor tenocytes. The results displayed enhanced cell proliferation ability at an early stage and an anti‐apoptotic effect on tenocytes, while treated with periostin and/or FGF7 proteins. Furthermore, there was a trend of promoted tenocyte migration capability. These findings indicated that Postn and FGF7 may represent novel cytokines to target flexor tendon healing.Clinical SignificanceThe preliminary discovery leads to a novel idea for treating tendinopathy in the musculoskeletal system using specific molecules identified from chordae tendineae.This article is protected by copyright. All rights reserved.
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BELMAHI, A. "La greffe tendineuse prot�g�e en zone 2Bou le pi�ge � fibroblastes." Chirurgie de la Main, May 2004. http://dx.doi.org/10.1016/s1297-3203(04)00039-3.
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Hsu, Yu‐Chen, Shi‐Feng Yang, Chia‐Lu Hung, Chia‐Jui Hung, Hsiang‐Po Huang, I‐Shing Yu, and Shu‐Wha Lin. "The role of serine protease in diaphragm development." FASEB Journal 31, S1 (April 2017). http://dx.doi.org/10.1096/fasebj.31.1_supplement.656.7.
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Congenital diaphragmatic hernias (CHD) are common birth defects that often have severe medical consequences. CHD occurs from the failure of diaphragm development, which leads to a herniation or elevation of abdominal components into the pleural cavity, and results in respiratory failure. Here we report that type II transmembrane serine protease‐1 (TMPRSS1)‐null mice exhibit defective diaphragms that mimic the phenotypes of the diaphragm elevation in humans. Histology and morphometry analyses showed that the tendinous muscle, but not the muscular layer in the diaphragm of the TMPRSS1‐null mice was significantly thinner than in the wild‐type mice. This phenomenon resulted in the position of the diaphragm and liver shifting upward, and the restricted expansion of the lung. We also observed that the pulmonary functions, such as lung resistance and compliance were also significantly impaired in the TMPRSS1‐null mice. To investigate the role of TMPRSS1 during the embryonic development of the diaphragm, we compared the area of diaphragm precursor structure, pleuroperitoneal folds (PPF) and the number of muscle progenitor cells and fibroblasts in the PPF between TMPRSS1‐null and wild‐type embryos (E13.5). The results showed that TMPRSS1‐null mice had no difference in the PPF area and the number of fibroblasts, while the number of muscle precursor cells was less than the wild type. These observations suggest that during early development, TMPRSS1 may play a role in maintaining the structure and function of the diaphragm and we would suggest that a genetic analysis of this modification be performed in patients with diaphragm elevation.
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Quam, Vivian G., Nadine N. Altmann, Matthew T. Brokken, and Sushmitha S. Durgam. "Zonal characterization and differential trilineage potentials of equine intrasynovial deep digital flexor tendon-derived cells." BMC Veterinary Research 17, no. 1 (April 1, 2021). http://dx.doi.org/10.1186/s12917-021-02793-1.
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Abstract Background Intrasynovial deep digital flexor tendon (DDFT) injuries occur frequently and are often implicated in cases of navicular disease with poor outcomes and reinjuries. Cell-based approaches to tendon healing are gaining traction in veterinary medicine and ultimately may contribute to improved DDFT healing in horses. However, a better understanding of the innate cellular characteristics of equine DDFT is necessary for developing improved therapeutic strategies. Additionally, fibrocartilaginous, intrasynovial tendons like the DDFT are common sites of injury and share a poor prognosis across species, offering translational applications of this research. The objective of this study is to isolate and characterize tendon-derived cells (TDC) from intrasynovial DDFT harvested from within the equine forelimb podotrochlear bursa. TDC from the fibrocartilaginous and tendinous zones are separately isolated and assessed. Flow cytometry is performed for mesenchymal stem cell (MSC) surface markers (CD 29, CD 44, CD 90). Basal tenogenic, osteogenic and chondrogenic markers are assessed via quantitative real time-PCR, and standard trilineage differentiation is performed with third passage TDC from the fibrocartilaginous (fTDC) and tendinous (tTDC) zones of DDFT. Results Low-density plating isolated homogenous TDC populations from both zones. During monolayer passage, both TDC subpopulations exhibited clonogenicity, high in vitro proliferation rate, and fibroblast-like morphology. fTDC and tTDC were positive for MSC surface markers CD90 and CD29 and negative for CD44. There were no significant differences in basal tenogenic, osteogenic or chondrogenic marker expression between zones. While fTDC were largely restricted to chondrogenic differentiation, tTDC underwent osteogenic and chondrogenic differentiation. Both TDC subpopulations displayed weak adipogenic differentiation potentials. Conclusions TDC at the level of the podotrochlear bursa, that potentially could be targeted for enhancing DDFT injury healing in horses were identified and characterized. Pending further investigation, promoting chondrogenic properties in cells administered exogenously into the intrasynovial space may be beneficial for intrasynovial tendon regeneration.
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Merrill, Amy Elizabeth, and Ryan Roberts. "Regulating Skeletal Progenitor Cells at the Interface Between Tendon and Bone." FASEB Journal 30, S1 (April 2016). http://dx.doi.org/10.1096/fasebj.30.1_supplement.83.4.
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The surfaces of bones are adorned with projections that mark their integration into the musculoskeletal system. These structures, known as bone eminences, take on diverse shapes and sizes to form anchoring points for tendons and ligaments. Bone eminences represent the mineralized side of the tendon‐bone attachment unit, which is composed of a transitional connective tissue, graded from tendinous to osseous. As such, the eminence plays a critical role transmitting forces generated by muscle contraction and dissipating stress concentrations across the hard‐soft tissue interface. During development, the tendon‐bone attachment unit descends from a unique pool of Scx+/Sox9+ progenitors that form secondary to those of the primary cartilage anlage and later become segregated into Scx+ tenocytes or Sox9+ chondrocytes of the eminence (Bltiz et al., 2009, 2013; Sugimoto et al., 2013). While many open questions remain about the molecular regulators that demarcate this boundary across the Scx+/Sox9+ progenitor field, chick embryo studies suggest a role for Fibroblast Growth Factor (FGF) signaling (Brent et al., 2003, 2004, 2005). We have uncovered evidence that Fgfr2 regulates cell fate choice during development of tendon‐bone attachment units in the craniofacial complex of mice. We have found that loss of Fgfr2 increases the eminence superstructure by promoting chondrogenic over tenocytic cell fate in the attachment unit progenitors. These findings contribute to the understanding of tendon‐bone attachment unit development and reveal a possible mechanism to explain the constellation of clinical abnormalities of the tendon‐bone interface that are found in the skeletal birth defects caused by gain and loss of FGFR2 function.Support or Funding InformationNIH, NIDCR #1R01DE025222 to A.E.M.March of Dimes, Gene Discovery and Translational Research Grant #6‐FY15‐233 to A.E.M.NIH, NIDCR #T90DE021982 to R.R.