Summary Background Slab fractures of the third carpal bone (C3) are a common injury of Thoroughbred racehorses. Results of arthroscopically guided repair have not been reported since the initial description of the technique in 1986. Additionally, fracture details and racing outcomes in a population of Thoroughbreds racing under UK jurisdiction have not previously been described. Objectives To report the frequency distribution of C3 slab fractures and to determine the impact on racing performance following arthroscopically guided repair in a population of Thoroughbred racehorses. Study design Retrospective case series. Methods Case records of Thoroughbred racehorses undergoing arthroscopically guided repair of C3 slab fractures at Newmarket Equine Hospital between 2006 and 2015 were retrieved. Radiographs and arthroscopic studies were reviewed. The effect of demography and fracture morphology on racing outcome was evaluated. Results C3 slab fractures occurred most commonly through the radial facet in a frontal plane (45/71 63.4%). Comminution was identified during arthroscopy in 42/71 (59.2%) fractures and occurred most frequently at the palmar margin of the fracture. Forty‐one out of 65 horses (63.1%) raced at least once post‐operatively. Females were less likely to return to racing compared to males (P<0.001). Horses that had raced before injury were more likely (OR 4.4, 95% CI 1.4–13.5, P = 0.01) to race after injury compared to horses that were unraced at the time of injury. After injury horses had a small but significant reduction in racing performance. Main limitations The series is a preselected population of Thoroughbred racehorses which referring veterinary surgeons considered potential candidates for surgical repair. Conclusion Fracture configurations can be identified radiographically but is not a reliable predictor of comminution or other intra‐articular lesions. Arthroscopy not only directs repair but also identifies and facilitates management of concurrent lesions. The results reported should assist in formulating appropriate prognoses for Thoroughbred horses racing in the UK.

In human, mutations of the protocadherins FAT4 and DCHS1 result in Van Maldergem syndrome, which is characterised, in part, by craniofacial abnormalities. Here, we analyse the role of Dchs1-Fat4 signalling during osteoblast differentiation in mouse. We show that Fat4 and Dchs1 mutants mimic the craniofacial phenotype of the human syndrome and that Dchs1-Fat4 signalling is essential for osteoblast differentiation. In Dchs1/Fat4 mutants, proliferation of osteoprogenitors is increased and osteoblast differentiation is delayed. We show that loss of Dchs1-Fat4 signalling is linked to increased Yap-Tead activity and that Yap is expressed and required for proliferation in osteoprogenitors. In contrast, Taz is expressed in more-committed Runx2-expressing osteoblasts, Taz does not regulate osteoblast proliferation and Taz-Tead activity is unaffected in Dchs1/Fat4 mutants. Finally, we show that Yap and Taz differentially regulate the transcriptional activity of Runx2, and that the activity of Yap-Runx2 and Taz-Runx2 complexes is altered in Dchs1/Fat4 mutant osteoblasts. In conclusion, these data identify Dchs1-Fat4 as a signalling pathway in osteoblast differentiation, reveal its crucial role within the early Runx2 progenitors, and identify distinct requirements for Yap and Taz during osteoblast differentiation.