Bone circulatory disturbances in the development of spontaneous bacterial chondronecrosis with osteomyelitis: a translational model for the pathogenesis of femoral head necrosis

Abstract

This review provides a comprehensive overview of the vascularization of the avian growth plate and its subsequent role in the pathogenesis of bacterial chondronecrosis with osteomyelitis (BCO, femoral head necrosis). BCO sporadically causes high incidences of lameness in rapidly growing broiler (meat-type) chickens. BCO is believed to be initiated by micro-trauma to poorly mineralized columns of cartilage cells in the proximal growth plates of the leg bones, followed by colonization by hematogenously distributed opportunistic bacteria. Inadequate blood flow to the growth plate, vascular occlusion, and structural limitations of the microvasculature all have been implicated in the pathogenesis of BCO. Treatment strategies have been difficult to investigate because under normal conditions the incidence of BCO typically is low and sporadic. Rearing broilers on wire flooring triggers the spontaneous development of high incidences of lameness attributable to pathognomonic BCO lesions. Wire flooring imposes persistent footing instability and is thought to accelerate the development of BCO by amplifying the torque and shear stress imposed on susceptible leg joints. Wire flooring per se also constitutes a significant chronic stressor that promotes bacterial proliferation attributed to stress-mediated immunosuppression. Indeed, dexamethasone-mediated immunosuppression causes broilers to develop lameness primarily associated with avascular necrosis and BCO. Prophylactic probiotic administration consistently reduces the incidence of lameness in broilers reared on wire flooring, presumably by reducing bacterial translocation from the gastrointestinal tract that likely contributes to hematogenous infection of the leg bones. The pathogenesis of BCO in broilers is directly relevant to osteomyelitis in growing children, as well as to avascular femoral head necrosis in adults. Our new model for reliably triggering spontaneous osteomyelitis in large numbers of animals represents an important opportunity to conduct translational research focused on developing effective prophylactic and therapeutic treatments.

Evaluating portable wire-flooring models for inducing bacterial chondronecrosis with osteomyelitis in broilers

“…Lesions associated with BCO can occur in all bones but are most commonly found in regions of the leg bones that have the widest growth plates and are subjected to torque and stress, such as the proximal tibiotarsus (tibia) and proximal head of the femur (Nairn, 1973;Wideman and Prisby, 2013). The pathogenesis of BCO is thought to be initiated by mechanical damage (e.g., osteochondrosis) to poorly mineralized columns of chondrocytes (cartilage cells) in the epiphyseal and physeal growth plates, followed by colonization of osteochondrotic clefts by hematogenously distributed opportunistic bacteria (Wise, 1971;Nairn, 1973;Howlett, 1980;Mutalib et al, 1983a;Thorp and Duff, 1988;Wideman and Prisby, 2013).…”

“…The pathogenesis of BCO is thought to be initiated by mechanical damage (e.g., osteochondrosis) to poorly mineralized columns of chondrocytes (cartilage cells) in the epiphyseal and physeal growth plates, followed by colonization of osteochondrotic clefts by hematogenously distributed opportunistic bacteria (Wise, 1971;Nairn, 1973;Howlett, 1980;Mutalib et al, 1983a;Thorp and Duff, 1988;Wideman and Prisby, 2013). Numerous bacterial species, including Staphylococcus spp., Escherichia coli, Mycobacterium avium, Salmonella spp., and Enterococcus spp., have been isolated from BCO lesions, with Staphylococcus aureus being routinely isolated over the course of several decades and across broad geographic distributions (Bradshaw et al, 2002).…”

Multifocal osteonecrosis and osteomyelitis in a liver transplant recipient

“…[20][21][22][23] On the other hand, in situations with bacteriemia, hematogenously distributed bacteria possessing the specific ability to bind to bone collagen and, has capacity to trigger osteomyelitis. [24,25] The bacteria adhere directly to the cartilage matrix and they form obstructive emboli in the metaphyseal vasculature causes local ischemia and necrosis. [24][25][26] In our patient uncontrolled biliary system infection may possibly lead to osteonecrosis and osteomyelitis as a result of hematogenous dissemination of bacteria.…”

“…[24,25] The bacteria adhere directly to the cartilage matrix and they form obstructive emboli in the metaphyseal vasculature causes local ischemia and necrosis. [24][25][26] In our patient uncontrolled biliary system infection may possibly lead to osteonecrosis and osteomyelitis as a result of hematogenous dissemination of bacteria.…”

Clinical effect of hyperbaric oxygen therapy in the treatment of femoral head necrosis

“…Its essence is death of bone cells in the complicated fractures, which can lead to the changes in bone, cause collapse of the bone fracture, and change the shape and function. Many studies have shown that one of the important factors causing bone cell apoptosis is blood supply to the femoral head [6][7][8]. Non-traumatic femoral head necrosis is divided into ischemic and idiopathic necrosis of the femoral head [9][10][11].…”