Objective—To evaluate early cellular influences of bone morphogenetic protein (BMP)12 and BMP2 on equine superficial digital flexor tenocytes (SDFTNs) and equine bone marrow–derived mesenchymal stem cells (BMDMSCs).
Animals—9 adult clinically normal horses.
Procedures—BMDMSCs and SDFTNs were cultured in monolayer, either untreated or transduced with adenovirus encoding green fluorescent protein, adenovirus encoding BMP12, or adenovirus encoding BMP2. Cytomorphologic, cytochemical, immunocytochemical, and reverse transcriptase–quantitative PCR (RT-qPCR) analyses were performed on days 3 and 6. Genetic profiling for effects of BMP12 was evaluated by use of an equine gene expression microarray on day 6.
Results—BMDMSCs and SDFTNs had high BMP12 gene expression and remained viable and healthy for at least 6 days. Type l collagen immunocytochemical staining for SDFTNs and tenocyte-like morphology for SDFTNs and BMDMSCs were greatest in BMP12 cells. Cartilage oligomeric matrix protein, as determined via RT-qPCR assay, and chondroitin sulfate, as determined via gene expression microarray analysis, were upregulated relative to control groups in SDFTN-BMP12 cells. The BMDMSCs and SDFTNs became mineralized with BMP2, but not BMP12. Superficial digital flexor tenocytes responded to BMP12 with upregulation of genes relevant to tendon healing and without mineralization as seen with BMP2.
Conclusions and Clinical Relevance—Targeted equine SDFTNs may respond to BMP12 with improved tenocyte morphology and without mineralization, as seen with BMP2. Bone marrow–derived mesenchymal stem cells may be able to serve as a cell delivery method for BMP12.
Objective—To determine survival rate and athletic ability after nonsurgical or surgical treatment of cleft palate in horses.
Design—Retrospective case series.
Animals—55 horses with cleft palate.
Procedures—13 of the 55 horses died or were euthanized without treatment and were not included in all analyses. Medical records were reviewed for signalment, history, method of diagnosis, soft or hard palate involvement, type of surgical procedure performed, postoperative complications, and survival to hospital discharge. Information on athletic ability was acquired from race records and follow-up conversations with owners, trainers, or referring veterinarians.
Results—The predominant reason for initial evaluation was milk or feed in the nostrils (60%). The diagnosis was confirmed by means of videoendoscopy of the upper portion of the airway in all cases. Most cases involved the soft palate only (92.7%). Twenty-six of the 55 (47.3%) horses underwent surgical repair, and 12 of these had dehiscence at the caudal edge of the soft palate. Among potential racehorses, 14 of 33 had surgery. Of these, 12 of 14 survived to discharge and 2 horses raced. Among potential racehorses, 10 of 33 were discharged without surgery and 2 of these raced. Among nonracehorses, 12 of 22 underwent surgery and 11 survived to discharge. All horses that were discharged and for which follow-up information was available survived to 2 years of age or older without ill thrift despite dehiscence at the caudal edge of the soft palate and continued mild nasal discharge.
Conclusions and Clinical Relevance—Horses with cleft palate had a higher survival rate than previously reported.