Osteochondrosis in the Distal Femoral Physis of Pigs Starts With Vascular Failure

Abstract

Articular osteochondrosis (OC) arises due to vascular failure and ischemic chondronecrosis. The aim of the study was to describe the histological and computed tomographic (CT) characteristics of changes in the distal femoral physis of pigs, to determine if they represented OC lesions and if the pathogenesis was the same as for articular OC. The material included 19 male Landrace pigs bred for predisposition to OC. One or 2 pigs were euthanized and CT-scanned at 2-week intervals from 82 to 180 days of age. Material from 10 pigs was available for histological validation. The CT scans revealed 31 lesions confirmed in 3 planes and 1 additional macroscopically visible lesion confirmed in 2 CT planes. Twelve of the lesions were histologically validated. All lesions were compatible with OC. Cartilage canal and eosinophilic streak morphological changes corresponded to failure of end arteries coursing from the epiphysis, toward the metaphysis. The location of lesions was compatible with failure at the point of vessel incorporation into bone. Vascular failure was associated with retention of viable hypertrophic chondrocytes and delayed ossification but not cartilage necrosis. Lesion width ranged from 1.1% to 45.6% of the physis. Several lesions were expected to resolve due to small size and evidence of CT-identifiable, reparative ossification. Angular limb deformity was not detected in any pig. The pathogenesis of physeal OC started with vascular failure that was morphologically identical to articular OC. The heritable predisposition may therefore be the same. The association between lesions and limb deformity should be studied further in older pigs in future.

Computed tomographic development of physeal osteochondrosis in pigs

“…The current results represent the longitudinal data from a project during which lesions in the right distal femoral physis of the included pigs were previously histologically validated [9]. In histological sections, lesions were centred on necrotic cartilage canal vessels and interpreted to represent vascular failure [9].…”

“…Articular osteochondrosis lesions can resolve or progress to pathologic fracture and OCD fragments in joints, associated with effusion, pain and lameness/leg weakness [1, 7, 8]. A recent cross-sectional study indicates that the pathogenesis of physeal osteochondrosis is similar to the pathogenesis of articular osteochondrosis [9]. Physeal lesions were also compatible with failure of end arteries at the point of incorporation into bone [9].…”

“…A recent cross-sectional study indicates that the pathogenesis of physeal osteochondrosis is similar to the pathogenesis of articular osteochondrosis [9]. Physeal lesions were also compatible with failure of end arteries at the point of incorporation into bone [9]. Devascularisation was associated with retention of viable hypertrophic chondrocytes, rather than necrosis, and focal delay in endochondral ossification/osteochondrosis [3, 9–11].…”

“…Physeal lesions were also compatible with failure of end arteries at the point of incorporation into bone [9]. Devascularisation was associated with retention of viable hypertrophic chondrocytes, rather than necrosis, and focal delay in endochondral ossification/osteochondrosis [3, 9–11]. The start of lesions: failure of vessels at the point of incorporation, and the effect: focal delay in ossification, were therefore the same for both physeal [9] and articular osteochondrosis [4, 5].…”

Lameness in fattening pigs – Mycoplasma hyosynoviae, osteochondropathy and reduced dietary phosphorus level as three influencing factors: A case report

“…In immature individuals, growth cartilage has a temporary blood supply in canals, which are later lled with cartilage (chondri cation) or are incorporated into the ossi cation front during process of maturation. Apoptotic chondrocytes can cause formation of lacunae, which might prevent osteoblast invasion and delaying ossi cation [11]. The etiology of osteochondrosis is mostly multifactorial, with several factors triggering disease development as heritable and anatomical traits and physical trauma, while rapid growth and dietary factors were also discussed [12].…”