History
An 11-month-old intact female Labrador Retriever–Poodle cross weighing 5.2 kg was presented to an academic referral hospital for further evaluation of a chronic progressive left hind limb lameness. Two months prior to presentation, the dog initially began intermittently limping on the left hind limb. There was no history of trauma. The dog was initially presented to the referring veterinarian and prescribed an NSAID (firocoxib, 5 mg/kg, PO, q 24 h for 4 weeks), gabapentin (10 mg/kg, PO, q 12 h for 2 weeks), and amantadine (3 mg/kg, PO, q 24 h, for 5 days). Pelvic radiographs were obtained at this time; however, no abnormalities were detected. The dog re-presented to the referring veterinarian 1 month later due to worsening of the lameness, which had progressed in severity. At this time, a CBC and biochemistry profile revealed no clinically significant findings. Referral was recommended.
On referral examination, the dog was bright, alert, and responsive with normal vital signs. General physical examination was unremarkable. A mild (grade 2/5) left hind limb lameness was noted when walking. When standing, the dog would intermittently lift the left hind limb. On orthopedic examination, there was marked muscle atrophy to the gluteal and quadricep muscles of the left hind limb. Marked discomfort was noted on extension of the left hip. No discomfort was noted on bilateral stifle palpation, with no effusions or instability present (negative tibial thrust). The dog had bilateral medial patella luxation (grade 1/4) with no retropatellar pain. Orthopedic examination was otherwise unremarkable.
Radiographs of the hips were obtained, including a ventrodorsal extended femur and frog-legged radiographs (Figure 1).
Ventrodorsal pelvic extended femur (A) and ventrodorsal frog leg (B) radiographs of an 11-month-old intact female 5.2-kg Labrador Retriever–Poodle cross presenting for a chronic and progressive left hind limb lameness. Radiographs obtained on presentation. Bar = 2.5 mm.
Citation: Journal of the American Veterinary Medical Association 2025; 10.2460/javma.24.08.0496
Radiographic Findings and Interpretation
The shape of the left femoral head was irregular (Figure 2). It showed a flattened curvature, which was independent of the normal flattening of the fovea capitis. There was a thickened and sclerotic neck in comparison to the right femur. A radiolucent defect was present on the proximal aspect left femoral head with an area of increased opacity (sclerosis) below. There was also lysis within the femoral head when compared to the left femoral head. There was widening of the joint space, and the center of the femoral head was positioned lateral to the dorsal acetabular rim (this may also have been influenced by radiographic positioning). At the cranial acetabular rim there was periarticular new bone formation. Assessment of muscle mass could not be appreciated on the preoperative radiographic views but could be noted on the postoperative radiographs (Figure 3). Differential diagnoses included Legg-Calvé-Perthes (LCP) disease (also known as avascular necrosis of the femoral head), osteochondrosis, unilateral hip dysplasia, or a congenital abnormality.
Ventrodorsal pelvic extended femur (A) and ventrodorsal frog leg (B) radiographs of the dog described in Figure 1 revealing a markedly remodeled left femoral head. A radiolucent defect at the proximal aspect of the femoral head is evident (yellow arrow). There is also lysis within the femoral head when compared to the left femoral head. The left joint space is widened with poor femoral coverage when compared to the right coxofemoral joint (white arrows). Mild periarticular new bone formation is noted at the cranial acetabular rim (black arrow). Widening of the left femoral neck is noted when compared to the right femoral neck.
Citation: Journal of the American Veterinary Medical Association 2025; 10.2460/javma.24.08.0496
An intraoperative image of the femoral head following femoral head and neck excision (A) and a postoperative ventrodorsal pelvic radiograph (B) of the dog described in Figure 1. The femoral head is markedly remodeled and irregular in appearance. The radiograph documents appropriate femoral head and neck ostectomy having been performed. Skin staples are present.
Citation: Journal of the American Veterinary Medical Association 2025; 10.2460/javma.24.08.0496
Treatment and Outcome
Under a general anesthetic the following day, a left femoral head and neck ostectomy was performed without complication (Figure 3). The patient recovered uneventfully and was discharged 3 days postoperatively with an NSAID (meloxicam, 0.1 mg/kg, PO, q 24 h for 4 weeks) and amantadine (3 mg/kg, PO, q 24 h for 4 weeks). At an 8-week telephone follow-up, the owner reported that the dog was back to normal off-lead exercise, with no noticeable lameness or discomfort. At a 6-month telephone follow-up, the dog was continuing to do well.
Histopathology of the femoral head revealed subchondral epiphyseal coagulative necrosis consistent with LCP disease (Figure 4).
A histology image of the femoral head (articular cartilage and epiphyseal bone) showing multifocal areas of osteonecrosis and fragmentation (black arrow) of the subchondral bone (2.5X) of the dog described in Figure 1. Areas of osteonecrosis and myelofibrosis (early granulation tissue) are noted (yellow arrow). H&E staining.
Citation: Journal of the American Veterinary Medical Association 2025; 10.2460/javma.24.08.0496
Comments
Legg-Calvé-Perthes disease, or avascular necrosis of the femoral head, is a developmental condition seen predominantly in small- and toy-breed dogs.1 Miniature Poodles and Terrier breeds are predisposed. Dogs often present before 11 months of age, and < 20% can be bilateral.1
The pathogenesis of LCP is thought to be due to a vascular insult to the proximal femoral epiphysis; however, its full etiology is not completely understood,2 and other mechanisms have also been proposed. In the early stages of the disease, avascular necrosis and ischemia of the trabeculae in the femoral head occur. Over time, as the femoral head weakens, fragmentation and collapse of the subchondral bone occur, subsequently resulting in collapse of the joint surface and overlying cartilage, with widening of the joint space and subsequent discomfort.1 The physis and metaphyseal region can also be subject to extensive remodeling.
Following this avascular phase, histopathology has demonstrated the presence of osteoblasts and fibrosis occurring3 through revascularization. The biphasic loss and regain of blood supply suggests a vascular origin of the disease. The blood supply to the femoral head is extraosseous, intracapsular, and intraosseus. However, in juvenile dogs, the proximal femoral epiphyseal vascular supply relies almost solely on vessels that originate from the synovial membrane inserting on the femur, potentially increasing its vulnerability in this age group. Likewise, in cats, the artery of the ligament of the head of the femur also contributes to epiphyseal blood supply, and this route may explain why LCP is not generally observed in cats.
Five radiographic grades have been described that range from early changes of widening of the joint space (grade 1) to late changes including fragmentation of the femoral head (grade 5).1 Computed tomography is more sensitive for detecting early pathology and is recommended when LCP is suspected and a definitive radiological diagnosis cannot be made.4 The importance of repeated radiographs is highlighted in this case, as no radiographic evidence of disease could be detected on the referring veterinarian’s radiographs taken early in the clinical presentation. Due to the radiolucent defect identified in the proximal femoral head, osteochondrosis was considered as a potential differential; however, given the rarity of osteochondrosis of the femoral head, this was considered unlikely.5 For interest, the excised femoral head was CT scanned postoperatively and revealed focal bone loss throughout the femoral head, inconsistent with an osteochondral fragment (Supplementary Figure S1).
Surgical treatment includes salvage options such as a total hip replacement or femoral head and neck excision. As is recommended, this femoral head was sent for histopathology, which revealed multifocal areas of osteonecrosis and fragmentation of the subchondral bone (Figure 4). Areas of osteonecrosis were replaced by early myelofibrosis, while in other areas this was more acute with fibrin occupying medullary spaces.
Supplementary Materials
Supplementary materials are posted online at the journal website: avmajournals.avma.org.
Acknowledgments
None reported.
Disclosures
The authors have nothing to disclose. No AI-assisted technologies were used in generation of this manuscript.
Funding
The authors have nothing to disclose.
ORCID
M. Simpson https://orcid.org/0000-0002-4153-6915
References
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Ljunggren G. Legg-Perthes disease in the dog. Acta Orthop Scand. 1967;38(suppl 95):1-79. doi:10.3109/ort.1967.38.suppl-95.01
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Mickelson MR, McCurnin DM, Awbrey BJ, Maynard JA, Martin RK. Legg-Calvé-Perthes disease in dogs: a comparison to human Legg-Culvé-Perthes disease. Clin Orthop Relat Res. 1981;(157):287-300. doi:10.1097/00003086-198106000-00039
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Gambardella PC, Bojrab MJ, Monet E. Legg-Calvé-Perthes disease in dogs. In: Bojrab MJ, ed. Disease Mechanisms in Small Animal Surgery. Lea & Febiger; 1993:804-807.
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Thak MA, Yoon HY, Jeong S. Early stage Legg-Calve-Perthes disease in a dog: clinical, surgical, radiological, computed tomography and histological findings. J Vet Clin. 2013;30(5):366-370.
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Castro PF, Unruh SM, Ferrigno CRA, Fantoni DT. What Is Your Diagnosis? Osteochondritis dissecans. J Am Vet Med Assoc. 2009;235(2):151-152. doi:10.2460/javma.235.2.151