A 15-month-old 6.5-kg (14.3-lb) castrated male Chihuahua–Miniature Schnauzer mix (per genetic testing)a was presented with a progressive 4-month history of intermittent non–weight-bearing lameness of the left pelvic limb. The dog had been rescued as a neonate with its eyes still closed and had no history of injury or trauma. The lameness, which had been localized to the hip joint, had been treated for 3.5 months with carprofen, methocarbamol, omega-3 fatty acids, vitamin E, eicosapentaenoic acid, and undenatured chicken type II collagen as well as 11 cold laser treatments. No corticosteroid drugs had ever been administered. A partial treatment response had been noted only while carprofen was administered continuously at a therapeutic dose.
On presentation, results of physical examination, CBC, and serum biochemical analysis were unremarkable and no comorbidities were noted. Orthogonal radiographs of the hip joints were obtained with the pelvic limbs extended (an Orthopedic Foundation for Animals position). A 100-mm marker was placed above and parallel to the radiography tabletop at the height of the left femoral head for magnification recalibration. Imaging revealed a 4-mm radiolucent lesion on the distal caudomedial aspect of the left femoral head (Figure 1). Subluxation of the 12-mm-diameter femoral head was measured to be 2 mm by use of comparisons to the head superimposition over the dorsal aspect of the contralateral acetabular rim and the distance from the medial-most aspect of the femoral head to the acetabular medial cortical wall. The inside diameter of the femoral medullary canal at the nutrient foramen was 7 mm, and the canal flare index1 was 1.30.
Ventrodorsal radiographic images of the hip joints (pelvic limbs extended) in a 15-month-old castrated male Chihuahua–Miniature Schnauzer mix. A—A 4-mm-diameter radiolucency (arrow) is visible at the distal caudomedial aspect of the left femoral head. No similar radiolucency is seen on the right side. B—A magnified portion of the radiograph in panel A shows a mottled radiodensity replacing cancellous bone in the femoral epiphysis and neck (arrow). A radiopaque, microgranular osseous pattern is visible in the proximal femoral medullary cancellous bone, extending to the nutrient foramen. This is a sign often encountered in bone infarcts owing to dystrophic calcification of nodules of necrotic fat and necrotic cancellous bone, both of which become more radiopaque than viable bone that is not fully mineralized.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Ventrodorsal radiographic images of the hip joints (pelvic limbs extended) in a 15-month-old castrated male Chihuahua–Miniature Schnauzer mix. A—A 4-mm-diameter radiolucency (arrow) is visible at the distal caudomedial aspect of the left femoral head. No similar radiolucency is seen on the right side. B—A magnified portion of the radiograph in panel A shows a mottled radiodensity replacing cancellous bone in the femoral epiphysis and neck (arrow). A radiopaque, microgranular osseous pattern is visible in the proximal femoral medullary cancellous bone, extending to the nutrient foramen. This is a sign often encountered in bone infarcts owing to dystrophic calcification of nodules of necrotic fat and necrotic cancellous bone, both of which become more radiopaque than viable bone that is not fully mineralized.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Ventrodorsal radiographic images of the hip joints (pelvic limbs extended) in a 15-month-old castrated male Chihuahua–Miniature Schnauzer mix. A—A 4-mm-diameter radiolucency (arrow) is visible at the distal caudomedial aspect of the left femoral head. No similar radiolucency is seen on the right side. B—A magnified portion of the radiograph in panel A shows a mottled radiodensity replacing cancellous bone in the femoral epiphysis and neck (arrow). A radiopaque, microgranular osseous pattern is visible in the proximal femoral medullary cancellous bone, extending to the nutrient foramen. This is a sign often encountered in bone infarcts owing to dystrophic calcification of nodules of necrotic fat and necrotic cancellous bone, both of which become more radiopaque than viable bone that is not fully mineralized.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Reevaluation at 2 months after the initial examination was recommended to allow examination of the entire left pelvic limb and lumbar portion of the vertebral column for definitive pain localization. The owner was instructed to monitor and record the dog's response at home to an initial therapeutic dosage of carprofen as well as when the dosage was tapered to an as-needed basis over the ensuing 2-week period. Surgical options to treat the lameness, including femoral head ostectomy and THR, were discussed with the owner but not recommended during the initial consultation because the radiographic bone changes were minimal, even though the dog had a non–weight-bearing lameness. Considerations regarding THR included the need to have a prosthetic femoral stem designed and manufactured because of the atypically large diameter of the medullary canal (low canal flare index) of the affected femur, at an unknown cost and unknown delay until surgery could be performed.
When the dog was returned 2 months after initial evaluation, no new orthopedic findings or neurologic abnormalities were observed other than signs of severe discomfort on hip joint manipulation. The radiographically visible lesion had increased in depth to 2 mm, and the diameter had increased from 4 to 6 mm. A cleft had become apparent between the subchondral and cancellous bone of the femoral head (Figure 2).
Ventrodorsal radiographic images of the hip joints (pelvic limbs extended) of the dog of Figure 1, as obtained 2 months later. A—The lesion in the left femoral head (arrow) has enlarged in diameter from 4 to 6 mm. B—A magnified portion of the radiograph in panel A shows the lesion (thin arrow) more clearly, including a positional shift of the partially detached osteochondral flap (thick arrow).
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Ventrodorsal radiographic images of the hip joints (pelvic limbs extended) of the dog of Figure 1, as obtained 2 months later. A—The lesion in the left femoral head (arrow) has enlarged in diameter from 4 to 6 mm. B—A magnified portion of the radiograph in panel A shows the lesion (thin arrow) more clearly, including a positional shift of the partially detached osteochondral flap (thick arrow).
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Ventrodorsal radiographic images of the hip joints (pelvic limbs extended) of the dog of Figure 1, as obtained 2 months later. A—The lesion in the left femoral head (arrow) has enlarged in diameter from 4 to 6 mm. B—A magnified portion of the radiograph in panel A shows the lesion (thin arrow) more clearly, including a positional shift of the partially detached osteochondral flap (thick arrow).
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Given these findings, the owner elected to have the dog undergo a THR procedure to provide a pain-free joint with normal biomechanics, without the risk of compromised function that might occur with femoral head ostectomy in an active dog. Surgery preplanning for implant size determination was completed on the basis of anatomic measurements of the hip joint on digital images. The images were recalibrated for magnification with software that recognized a 100-mm magnification marker on a magnification marker stand with the marker at the height of the left femoral head at image capture. The inside diameter of the left acetabulum between subchondral bone at the cranial and caudal poles measured 15 mm. A 14-mm acetabular cupb was determined to be the correct size. A custom #4 cobalt chrome femoral component with a 4.6-mm stem tip was orderedc to create a better fit in the 7-mm-diameter femoral canal. The trunnion on the stem was custom fabricated for use with an 8-mm femoral head and designed to mimic the trunnion diameter of the #3 stem but with a 2-mm increase in femoral neck length.
The evening prior to surgery, the dog was admitted to the hospital and a fentanyl patch (25 μg/h) was placed on the ventral thoracic region caudal to the axilla until removed 72 hours after surgery. The anesthetic protocol consisted of premedication with hydromorphone hydrochloride (0.1 mg/kg [0.045 mg/lb], IM) and glycopyrrolate (0.02 mg/kg [0.009 mg/lb], IM), followed by propofol induction (4 mg/kg [1.8 mg/lb], IV, titrated to effect) and maintenance of anesthesia with isoflurane. A constant rate IV infusion of morphine, lidocaine, and ketamine was provided during and after surgery for analgesia and sedation. Amikacin (15 mg/kg [6.8 mg/lb], slowly IV) and cefazolin (4.5 mg/kg [2.0 mg/lb], IV, q 90 min throughout surgery) were administered at anesthetic induction.
Surgery, which involved polymethyl methacrylate bone cementd fixation, was performed as a micro-THRc procedure as previously described.2 The excised native femoral head (Figure 3) and contiguous portion of the femoral neck were immediately placed in neutral-buffered 10% formalin (pH, 6.95 to 7.05) for preservation and later histologic evaluation. The round ligament was found to be completely torn. Total durations of anesthesia (from induction to extubation) and surgery were 169 and 87 minutes, respectively.
Photograph of the excised femoral head from the THR procedure for the dog of Figure 1 (scale in centimeters). The osteochondral flap (arrowheads) is visible. The margins of the osteochondral flap appear collapsed owing to bone necrosis and loss of support in the subchondral epiphyseal substantia spongiosa. The insertion site of the round ligament (arrow) on the head of the femur was no longer intact and was smooth. The proximodorsal aspect of the intact articular surface area of the femoral head is also visible (asterisk).
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Photograph of the excised femoral head from the THR procedure for the dog of Figure 1 (scale in centimeters). The osteochondral flap (arrowheads) is visible. The margins of the osteochondral flap appear collapsed owing to bone necrosis and loss of support in the subchondral epiphyseal substantia spongiosa. The insertion site of the round ligament (arrow) on the head of the femur was no longer intact and was smooth. The proximodorsal aspect of the intact articular surface area of the femoral head is also visible (asterisk).
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Photograph of the excised femoral head from the THR procedure for the dog of Figure 1 (scale in centimeters). The osteochondral flap (arrowheads) is visible. The margins of the osteochondral flap appear collapsed owing to bone necrosis and loss of support in the subchondral epiphyseal substantia spongiosa. The insertion site of the round ligament (arrow) on the head of the femur was no longer intact and was smooth. The proximodorsal aspect of the intact articular surface area of the femoral head is also visible (asterisk).
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
After surgery, a continuous rate IV infusion of dexmedetomidine was provided at a rate of 1 μg/kg/h (0.45 μg/lb/h) for 8 hours as needed for sedation. Postoperative radiography of the hip joints revealed that the cup angle of the lateral opening was 60°. The angle of femoral neck anteversion was 1° (Figure 4).
Lateral (A) and ventrodorsal (B) radiographic images of the left hip joint in the dog of Figure 1 as obtained immediately after the THR procedure, showing the prosthesis rearticulation. Images show a wire ring embedded in the 14-mm acetabular cup, the custom #4 femoral stem, and an 8-mm femoral head with a 2-mm neck-length extension.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Lateral (A) and ventrodorsal (B) radiographic images of the left hip joint in the dog of Figure 1 as obtained immediately after the THR procedure, showing the prosthesis rearticulation. Images show a wire ring embedded in the 14-mm acetabular cup, the custom #4 femoral stem, and an 8-mm femoral head with a 2-mm neck-length extension.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Lateral (A) and ventrodorsal (B) radiographic images of the left hip joint in the dog of Figure 1 as obtained immediately after the THR procedure, showing the prosthesis rearticulation. Images show a wire ring embedded in the 14-mm acetabular cup, the custom #4 femoral stem, and an 8-mm femoral head with a 2-mm neck-length extension.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Beginning the morning after surgery, oral administration of tramadol, carprofen, and cefpodoxime was initiated and continued for 5 days. The dog was discharged from the hospital the next day with a prescription for acepromazine maleate (5 mg, PO, as needed for sedation for up to 10 days) and instructions for the owner to restrict the dog's activity for 6 weeks to surfaces with good traction when indoors and to provide leash control when outdoors for elimination purposes. During that time, no running, jumping, playing, stair climbing or descending, or walks other than for elimination purposes were to be allowed.
At 6 weeks after surgery, the dog was returned for reevaluation. Radiographic findings confirmed stable implant fixation with no complications. The owner was instructed to provide walks on a leash twice a day for the next 30 days, with the duration, distance, and speed progressively increasing from a slow 10-minute walk to a fast walk for approximately 20 minutes. Normal indoor activity was allowed to resume 10 days after walking exercise began. All normal outdoor activity was allowed to resume 3 months after surgery.
Histologic evaluation of the femoral head lesion revealed distortion of the articular surface that was characterized by variable thickening and thinning of the cartilage. Chondrocyte polarity disruption was present in the worst-affected areas. Small nests of cartilage appeared suspended in subjacent cancellous bone. Small articular cartilage fissures and fractures accounted for the discontinuities. No inflammatory changes or signs of infectious disease or neoplasia were noted. Findings indicated that remodeling of the epiphyseal cancellous bone during a period of progressive bone infarction preceded subchondral bone necrosis and fragmentation. Necrotic subchondral epiphyseal spongiosa that collapsed beneath intact subchondral bone resulted in a partially attached osteochondral flap. The lesions were consistent with an idiopathic arteriopathy that had created infarction of the femoral head (Figure 5).
Photomicrographs of sections of the excised femoral head from the dog of Figure 1. A—A completely formed and intact subchondral bone plate (thin red arrow) represents normal formation of the articular surface. Distortion and thinning of the articular cartilage over the subchondral lesion are evident on the left. The pathological fracture line is interposed through the superficial lesion and, in this image, dissects along the superficial cancellous bone support for the subchondral bone plate. Disorganized remodeled structurally weakened necrotic cancellous bone led to mechanical failure of the articular surface support during weight-bearing. Nests of cartilage (double-headed black arrow) in the still-attached fragment of ischemic subchondral bone and adjacent surface of cancellous bone reflect aborted attempts at repair. The pathological fracture line and cleft (wide red arrow) in the subchondral plate pass between a partially attached osteochondral fragment and the surface of the necrotic epiphyseal substantia spongiosa. The infarcted cancellous bone (wide black arrow) became distorted during abortive attempts at repair until infarction became complete. The necrotic fatty marrow in this haphazard filigree of cancellous bone was replaced by ischemic fibrous tissue. A cartilage fissure and elevation of the articular surface (double-headed white arrow) was allowed to happen owing to loss of supporting subchondral cancellous bone at the initial site of the fracture line. B—A small muscular artery (arrow) with an empty lumen is present, as is fibrosis of the adventitia and bordering ischemic adipose cells of the epiphysis. C—The medial epiphyseal infarct has small muscular arteries (arrows) with degenerative walls and collapsed lumens bordered by ischemic degenerative adipose tissue and hemorrhage. H&E stain; 20X (A) and 200X (B and C) magnification.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Photomicrographs of sections of the excised femoral head from the dog of Figure 1. A—A completely formed and intact subchondral bone plate (thin red arrow) represents normal formation of the articular surface. Distortion and thinning of the articular cartilage over the subchondral lesion are evident on the left. The pathological fracture line is interposed through the superficial lesion and, in this image, dissects along the superficial cancellous bone support for the subchondral bone plate. Disorganized remodeled structurally weakened necrotic cancellous bone led to mechanical failure of the articular surface support during weight-bearing. Nests of cartilage (double-headed black arrow) in the still-attached fragment of ischemic subchondral bone and adjacent surface of cancellous bone reflect aborted attempts at repair. The pathological fracture line and cleft (wide red arrow) in the subchondral plate pass between a partially attached osteochondral fragment and the surface of the necrotic epiphyseal substantia spongiosa. The infarcted cancellous bone (wide black arrow) became distorted during abortive attempts at repair until infarction became complete. The necrotic fatty marrow in this haphazard filigree of cancellous bone was replaced by ischemic fibrous tissue. A cartilage fissure and elevation of the articular surface (double-headed white arrow) was allowed to happen owing to loss of supporting subchondral cancellous bone at the initial site of the fracture line. B—A small muscular artery (arrow) with an empty lumen is present, as is fibrosis of the adventitia and bordering ischemic adipose cells of the epiphysis. C—The medial epiphyseal infarct has small muscular arteries (arrows) with degenerative walls and collapsed lumens bordered by ischemic degenerative adipose tissue and hemorrhage. H&E stain; 20X (A) and 200X (B and C) magnification.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Photomicrographs of sections of the excised femoral head from the dog of Figure 1. A—A completely formed and intact subchondral bone plate (thin red arrow) represents normal formation of the articular surface. Distortion and thinning of the articular cartilage over the subchondral lesion are evident on the left. The pathological fracture line is interposed through the superficial lesion and, in this image, dissects along the superficial cancellous bone support for the subchondral bone plate. Disorganized remodeled structurally weakened necrotic cancellous bone led to mechanical failure of the articular surface support during weight-bearing. Nests of cartilage (double-headed black arrow) in the still-attached fragment of ischemic subchondral bone and adjacent surface of cancellous bone reflect aborted attempts at repair. The pathological fracture line and cleft (wide red arrow) in the subchondral plate pass between a partially attached osteochondral fragment and the surface of the necrotic epiphyseal substantia spongiosa. The infarcted cancellous bone (wide black arrow) became distorted during abortive attempts at repair until infarction became complete. The necrotic fatty marrow in this haphazard filigree of cancellous bone was replaced by ischemic fibrous tissue. A cartilage fissure and elevation of the articular surface (double-headed white arrow) was allowed to happen owing to loss of supporting subchondral cancellous bone at the initial site of the fracture line. B—A small muscular artery (arrow) with an empty lumen is present, as is fibrosis of the adventitia and bordering ischemic adipose cells of the epiphysis. C—The medial epiphyseal infarct has small muscular arteries (arrows) with degenerative walls and collapsed lumens bordered by ischemic degenerative adipose tissue and hemorrhage. H&E stain; 20X (A) and 200X (B and C) magnification.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Follow-up radiography performed 13 months after surgery revealed stable implants, unchanged implant positioning, secure bone-cement interfaces, normal periprosthetic bone quality, no indication of implant wear, and no other problems. The contralateral hip joint continued to be unremarkable at that time. Follow-up telephone conversations with the owner 15 and 18 months after surgery confirmed that there were no signs of problems with freedom of activity, which was allowed both indoors and outdoors.
Discussion
Signs of pain in the hip region should be evaluated during orthopedic examination of young dogs that are suspected to have hip dysplasia, capital physeal fracture, LCPD, or other hip joint abnormalities. Radiography is usually chosen as the initial diagnostic test to evaluate hip joints. Focal osteonecrosis of the femoral head with subchondral fracture resulting in an articular surface–collapsing osteochondral lesion had not previously been reported in dogs, to the authors’ knowledge. In humans, however, nontraumatic ischemic osteonecrosis of the femoral head is a well-established diagnosis.3 Comparative research involving experimentally induced osteonecrosis of the femoral head in laboratory animals has been conducted to better understand the pathobiology of this disease.4 It is possible that FONFH has been overlooked as a definitive diagnosis in dogs because insufficient attention has been focused on this possibility. Focal osteonecrosis of the femoral head may also have been misdiagnosed as some other more familiar disease, such as avascular necrosis of the femoral head (LCPD) or OCD, but the classic locations and etiology are different and such lesions could be misclassified without histologic evaluation.
Femoral head osteonecrosis is idiopathic in approximately 30% of affected humans; therefore, the approach to treatment in humans is multifactorial.5 Alcohol consumption has long been known to be a risk factor for nontraumatic osteonecrosis.6 Other possible causes or factors include but are not limited to insufficient acetabular femoral head coverage,7 impingement disorders that compromise blood supply,8 and high-dose corticosteroid regimens.9 Iatrogenic disruption and compromise of the femoral head blood supply can occur during the reaming process for femoral head resurfacing arthroplasty, which can subsequently increase the risk of implant failure.10 Primary spontaneous osteonecrosis of the knee joint also occurs in humans.11
A revised version of an international staging system for osteonecrosis of the femoral head was published in 2020.12 In humans, irreversible slow progression of the degenerative process is typical, but osteonecrosis can also be a rapidly progressive arthritic condition.13 The femoral subcapital area is a common site for subchondral fracture secondary to osteonecrosis.14 Affected humans are often young and active with multiple initial salvage treatment options attempted, but THR is the most common option to resolve pain and allow return to normal function.15
The initial radiographic appearance of FONFH in humans is a radiolucent lesion under the articular surface between subchondral bone and cancellous bone. The lesion may be asymptomatic and could easily be overlooked in the early stages of development. When a small focal lesion is present, a presumptive diagnosis can be made radiographically but confirmation of the diagnosis is made by histologic evaluation.12–14 In dogs, FONFH could easily be mistakenly diagnosed as avascular necrosis of the femoral head, which is commonly seen in dogs,16 or OCD of the femoral head, which appears to be a rare disorder.17–19
To the authors’ knowledge, a focal pathological fracture in the epiphyseal subchondral bone of the distal caudomedial aspect of the femoral head caused by infarction of the epiphyseal spongiosa due to an idiopathic arteriopathy in a dog has not been reported; therefore, it has not been reported as a specific indication for THR surgery. Total hip replacement can allow small dogs to return to normal function with a pain-free joint.20 An alternative surgical procedure for dogs with signs of pain in a hip joint could be femoral head ostectomy, but this procedure has been reported to have a high (42%) incidence of unsatisfactory results at a mean of 4 years after surgery, as determined through objective outcome measurements.21
Osteochondritis dissecans and avascular necrosis of the femoral head (LCPD) were initially considered among the differential diagnoses for the dog of the present report. Both conditions can share some radiographic and gross similarities to the dog's lesions.22–24 However, the dog's lesions had a different pathogenesis (as identified by means of histologic findings), histopathologic features, distribution, and, especially, anatomic location.
Osteochondritis dissecans was considered on the basis of the gross appearance of the osteochondral flap in the dog, even though a diagnosis of OCD is made primarily in large-breed, typically 6- to 10-month-old dogs with a larger focal radiolucency. With OCD, a focal area of thickened articular cartilage on the weight-bearing surface of a joint becomes disrupted at the zonal interface of the osteochondral junction during endochondral ossification. This results in a separation at the interface where epiphyseal vessels invade the mineralization zone. Osteocytes and chondrocytes are both involved in the articular epiphyseal complex of the expanding secondary center of ossification of the epiphysis during skeletal development. The disruption causes a varying extent and depth of necrosis. The osteonecrosis at this weakened interface with the rotary and compressive forces during weight-bearing results in a fissure or cleft.22 The cleft leads to deformation of the loose, overlying osteochondral flap, which is the pathological feature referred to as osteochondritis dissecans. Therefore, OCD is a complication of a developmental disorder of osteochondrosis. Osteochondritis dissecans will progress to arthritis if undiagnosed or left untreated.25 Osteochondritis is actually a misnomer because inflammation of the bone is not a histopathologic feature of this disorder, even though synovitis is a characteristic finding in dogs with lameness.
Histopathologic findings indicated that the dog of the present report had an intact subchondral bone plate prior to fracture occurrence, indicating that endochondral ossification of the articular cartilage had been completed. Consequently, the dog did not have a developmental OCD bone lesion secondary to osteochondrosis.
The possibility of avascular necrosis of the femoral head (LCPD) was also considered for the dog of the present report. This disorder initially arises in the developing epiphysis beneath the acetabular rim, where compression is applied to the developing cartilage, the zone of endochondral ossification, and the epiphyseal blood supply in the developing dorsolateral aspect of the femoral head.23,24 The site of the initial lesion in the femoral head in dogs with avascular necrosis is therefore on the proximal dorsolateral aspect of the femoral head and not the opposite (distal caudomedial) aspect, as in the dog of the present report.
As supported by the histopathologic findings, the FONFH in the dog was due to focal infarction in the epiphyseal and femoral neck metaphyseal cancellous bone spongiosa. The blood supply to these structures is initially separate until after physeal plate closure. The pattern of avascular involvement in the dog indicated that an arteriopathy had affected both the metaphyseal and epiphyseal arterioles that provide blood supply to these structures in the distal caudomedial location prior to physeal plate closure (Figure 6). Infarction was due to degenerative arterioles present in both locations.
Illustration of the blood supply to the caudal femoral head metaphysis and epiphysis (caudal-to-cranial view) of the proximal aspect of the left femur (A) and an example of a microangiogram obtained in the same orientation (B). The medial circumflex artery supplies a posterior inferior branch to the distal caudomedial area of the epiphysis. The microangiogram shows the complexity of the circulation from the posterior inferior branch (arrow) to the area affected in the dog of Figure 1. Microangiography would not have been possible for the dog because of the occlusion caused by the arteriopathy.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Illustration of the blood supply to the caudal femoral head metaphysis and epiphysis (caudal-to-cranial view) of the proximal aspect of the left femur (A) and an example of a microangiogram obtained in the same orientation (B). The medial circumflex artery supplies a posterior inferior branch to the distal caudomedial area of the epiphysis. The microangiogram shows the complexity of the circulation from the posterior inferior branch (arrow) to the area affected in the dog of Figure 1. Microangiography would not have been possible for the dog because of the occlusion caused by the arteriopathy.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Illustration of the blood supply to the caudal femoral head metaphysis and epiphysis (caudal-to-cranial view) of the proximal aspect of the left femur (A) and an example of a microangiogram obtained in the same orientation (B). The medial circumflex artery supplies a posterior inferior branch to the distal caudomedial area of the epiphysis. The microangiogram shows the complexity of the circulation from the posterior inferior branch (arrow) to the area affected in the dog of Figure 1. Microangiography would not have been possible for the dog because of the occlusion caused by the arteriopathy.
Citation: Journal of the American Veterinary Medical Association 257, 9; 10.2460/javma.257.9.937
Histopathologic findings confirmed that the FONFH-related subchondral fracture was a pathological fracture caused by the bone infarction that had resulted from the observed idiopathic arteriopathy. Findings at the distal caudomedial aspect of the femoral head indicated that partial avulsion of the articular cartilage had occurred because of focal displacement after the cartilage had lost its base of support from the chronically remodeled, collapsed, and necrotic superficial epiphyseal spongiosa. The areas of intact subchondral bone plate indicated that endochondral ossification of the developing articular surface had been complete before the fracture occurred. Degenerate arterioles were observed to be seated in necrotic fatty marrow in ischemic epiphyseal spongiosa. Other similar effete arterioles were present in the infarcted metaphyseal spongiosa. Histologically similar arteriolar lesions causing osteonecrosis have been produced in laboratory mice by addition of dexamethasone to their drinking water.26 To the authors’ knowledge, the association between corticosteroid drugs and idiopathic arteriolar lesions resulting in bone infarcts has not been investigated in dogs and warrants exploration.
The dog of the present report had no known history of trauma, but hip joint laxity was present and the round ligament was not intact. Despite the lack of overt trauma, acute round ligament failure without luxation could not be totally ruled out. High intra-articular pressure can compress the hip joint and synovial membrane blood vessels to the degree that blood flow dwindles, resulting in bone ischemia.4 Another possibility that could not be eliminated was a subclinical traumatic event that had caused high intra-articular pressure from hemorrhage or laceration of small vessels.
Histopathologic findings suggested that the transverse subchondral bone fracture in the dog of the present report occurred after the subchondral bone plate had been formed and not during an earlier developmental period when the fracture line would have traversed a site of endochondral ossification. The mechanical forces applied to the surface over necrotic, weakened, subchondral epiphyseal cancellous bone resulted in collapse and fracture development. The possibility existed that the cancellous bone was undergoing revascularization and remodeling during the period of progressive infarction. Histologic evaluation revealed partial avulsion of the articular cartilage due to focal displacement after the cartilage had lost its base of support from the chronically remodeled, collapsed, and necrotic superficial epiphyseal spongiosa. The areas of intact subchondral bone plate indicated that endochondral ossification of the developing articular surface had been completed before the fracture occurred.
Magnetic resonance imaging and high-resolution CT have been used for staging or classification of osteonecrosis and for comparison to other femoral head abnormalities in humans.27 Arthroscopy allows visualization of articular lesions without the need for arthrotomy but does not provide a permanent resolution. In human medicine, osteochondral allografts have been used to treat similar lesions but are associated with a high incidence of arthritis progression and ultimately the need to convert to a THR procedure.28 Femoral head and neck fenestration through a direct approach combined with a compacted autograft implanted during the early disease stages may have promise for humans with nontraumatic osteonecrosis of the femoral head.29 Total hip replacement is the reliable treatment option for osteonecrosis of the hip joint, which has been difficult to treat in humans.30
For the dog of the present report, arthroscopic treatment and allograft transplantation or compacted grafting would have been technically challenging owing to the small size of the dog, the location and shape of the lesion, and ultimately the absence of a healthy blood supply for graft survival and healing. Diagnostic and treatment options other than THR might have been considered. Such options should be kept in mind in the future when discussing treatment alternatives with the owners. In the authors’ opinion, a treatment approach other than THR would have been unlikely to yield a better outcome than that achieved with THR, which was graded excellent by the owner 20 months after surgery. Therefore, THR should be considered for dogs with signalment and clinical findings similar to the dog of the present report until superior diagnostic testing and treatment options have been established.
Believed to be unrelated to the lesion, another feature of the dog was a disproportionately large proximal femoral medullary canal. Custom-made prostheses are feasible when patients have atypical anatomy and readily available commercial implants do not provide the best fit, as was true for the dog of the present report. A decision was made during the surgical preplanning stage to wait for a custom-manufactured prosthetic femoral stem that would provide the right fit and canal fill instead of using an available stem with the potential for complications such as aseptic loosening or metal fatigue and failure due to improper sizing. The additional 2-mm neck length of the custom stem reduced the probability of needing to extend the neck length by means of the femoral head lengthening option to achieve a secure rearticulation.
In conclusion, the present report represented the first description of FONFH with subchondral collapse due to an idiopathic arteriopathy involving the femoral head in a dog, to the authors’ knowledge. The definitive diagnosis can only be established by histologic examination of affected bone prior to the onset of adulthood or shortly thereafter before advanced degenerative changes develop. The diagnosis is not a gross or radiographic diagnosis, and the condition is not the same as OCD or LCPD. We hope that this report will heighten awareness among clinicians who examine hip joints in dogs, including general practitioners, radiologists, surgeons, and pathologists. Such awareness may lead to an earlier and more frequent definitive diagnosis. The described disease may develop in dogs more often than has been previously identified or even considered. As the disease progresses, the diagnosis could easily be missed or erroneously interpreted as idiopathic degenerative arthritis, unilateral hip dysplasia, or some other diagnostic terms used to describe advanced osteoarthritic changes. When radiographic lesions similar to the ones reported here are identified in the femoral head of a young dog, we believe the treatment approach most likely to produce a good outcome is currently THR. To heighten awareness and better understand FONFH in dogs, we recommend histologic evaluation of the femoral head for dogs when the underlying cause of pain and lameness attributable to the hip joint cannot be definitively established and is based solely on a radiographic diagnosis.
Acknowledgments
No third-party funding or support was received in connection with this case or the writing or publication of the manuscript. The authors declare that there were no conflicts of interest.
The uniqueness of the gross lesion in the dog was an observation made by the surgeons, but the discovery of the unique pathological diagnosis was made by the veterinary pathologist (Dr. Pool).
ABBREVIATIONS
| FONFH | Focal osteonecrosis of the femoral head |
| LCPD | Legg-Calvé-Perthes disease |
| OCD | Osteochondritis dissecans |
| THR | Total hip replacement |
Footnotes
Genetic Health Analysis, Mars Inc, McLean, Va.
CFX acetabular cup, BioMedtrix LLC, Whippany, NJ.
BioMedtrix LLC, Whippany, NJ.
Palacos LV, Zimmer, Warsaw, Ind.
References
1. Rashmir-Raven AM, DeYoung DJ, Abrams CF Jr, et al. Subsidence of an uncemented canine femoral stem. Vet Surg 1992;21:327–331.
2. Liska WD. Micro total hip replacement for dogs and cats: surgical technique and outcomes. Vet Surg 2010;39:797–810.
3. Bradway JK, Morrey BF. The natural history of the silent hip in bilateral atraumatic osteonecrosis. J Arthroplasty 1993;8:383–387.
4. Boss JH, Misselevich I. Osteonecrosis of the femoral head of laboratory animals: the lessons learned from the comparative study of osteonecrosis in man and experimental animals. Vet Pathol 2003;40:345–354.
5. Stulberg BN. Osteonecrosis: what to do, what to do! J Arthroplasty 2003;18:74–79.
6. Yoon BH, Jones LC, Chen CH, et al. Etiologic classification criteria of ARCO on femoral head osteonecrosis part 2: alcohol-associated osteonecrosis. J Arthroplasty 2019;34:169–174.
7. Kang JS, Park S, Song JH, et al. Prevalence of osteonecrosis of the femoral head: a nationwide epidemiologic analysis in Korea. J Arthroplasty 2009;24:1178–1183.
8. Clohisy J, Robison J, Callaghan J, et al. Defining the etiologies of premature hip joint degeneration: do impingement disorders have a role? J Arthroplasty 2008;23:325.
9. Mont MA, Pivec R, Banerjee S, et al. High-dose corticosteroid use and risk of hip osteonecrosis: meta-analysis and systematic literature review. J Arthroplasty 2015;30:1506–1512.
10. Dy CJ, Thompson MT, Usrey MM, et al. The distribution of vascular foramina at the femoral head/neck junction: implications for resurfacing arthroplasty. J Arthroplasty 2012;27:1669–1675.
11. Lieberman JR, Varthi AG, Polkowski GG. Osteonecrosis of the knee—which joint preservation procedures work? J Arthroplasty 2014;29:52–56.
12. Yoon BH, Mont MA, Koo KH, et al. The 2019 revised version of Association Research Circulation Osseous staging system of osteonecrosis of the femoral head. J Arthroplasty 2020;35:933–940.
13. Mesko JW. Rapidly progressive femoral head osteolysis. J Arthroplasty 1993;8:541–547.
14. Lee JS, Suh KT. A pathological fracture of the femoral neck associated with osteonecrosis of the femoral head and a stress fracture of the contralateral femoral neck. J Arthroplasty 2005;20:807–810.
15. Brinker MR, Rosenberg AG, Kull L, et al. Primary total hip arthroplasty using noncemented porous-coated femoral components in patients with osteonecrosis of the femoral head. J Arthroplasty 1994;9:457–468.
16. Jankovits DA, Liska WD, Kalis RH. Treatment of avascular necrosis of the femoral head in small dogs with micro total hip replacement. Vet Surg 2012;41:143–147.
17. Johnson AL, Pijanowski GJ, Stein LE. Osteochondritis dissecans of the femoral head of a Pekingese. J Am Vet Med Assoc 1985;187:623–625.
18. McDonald M. Osteochondritis dissecans of the femoral head: a case report. J Small Anim Pract 1988;29:49–53.
19. Castro PF, Unruh SM, Ferrigno CRA, et al. What Is Your Diagnosis? Osteochondritis dissecans. J Am Vet Med Assoc 2009;235:151–152.
20. Budsberg SC, Chambers JN, Lue SL, et al. Prospective evaluation of ground reaction forces in dogs undergoing unilateral total hip replacement. Am J Vet Res 1996;57;1780–1785.
21. Off W, Matis U. Excision arthroplasty of the hip joint in dogs and cats. Clinical, radiographic, and gait analysis findings from the Department of Surgery, Veterinary Faculty of the Ludwig-Maximilians-University of Munich, Germany. 1997. Vet Comp Orthop Traumatol 2010;23:297–305.
22. Accadbled F, Vial J, Sales de Gauzy J. Osteochondritis dissecans of the knee. Orthop Traumatol Surg Res 2018;104:S97–S105.
23. Catterall A. Pathology and classification. Hip 1985;12:6.
24. Kollitz KM, Gee AO. Classifications in brief: the Herring lateral pillar classification for Legg-Calvé-Perthes disease. Clin Orthop Relat Res 2013;471:2068–2072.
25. Demko J, McLaughlin R. Developmental orthopedic disease. Vet Clin North Am Small Anim Pract 2005;35:1111–1135.
26. Janke LJ, Liu C, Vogel P, et al. Primary epiphyseal arteriopathy in a mouse model of steroid-induced osteonecrosis. Am J Pathol 2013;183:19–25.
27. Zizic TM. Osteonecrosis. Curr Opin Rheumatol 1991;3:481–489.
28. Mei XY, Alshaygy IS, Safir OA, et al. Fresh osteochondral allograft transplantation for treatment of large cartilage defects of the femoral head: a minimum two-year follow-up study of twenty-two patients. J Arthroplasty 2018;33:2050–2056.
29. Wang Q, Li D, Yang Z, et al. Femoral head and neck fenestration through a direct anterior approach combined with compacted autograft for the treatment of early stage nontraumatic osteonecrosis of the femoral head: a retrospective study. J Arthroplasty 2020;35:652–660.
30. Issa K, Pivec R, Kapadia BH, et al. Osteonecrosis of the femoral head: the total hip replacement solution. Bone Joint J 2013;95:46–50.
