Summary Forelimb navicular bones and associated soft tissues were collected from 3 groups of horses and subjected to pathological examinations. The groups consisted of 38 horses with clinical navicular disease (ND) and 2 control groups, with no history of forelimb lameness, consisting of 25 age‐matched mature horses (A‐MC) and 9 immature horses (IC). Histological and histomorphometric studies were performed on tissue samples from 10 ND, 10 A‐MC and 5 IC horses. Gross changes seen only in ND horses included: full thickness defects in the palmar surface fibrocartilage, palmar cortex erosion, medullary lysis, flexor digitorum profundus tendon (FDPT) surface fibrillation, FDPT core lesions and adhesions between the FDPT and navicular bone. Palmar surface partial thickness fibrocartilage loss and distal border fragmentation were seen with a significantly greater incidence in ND than in A‐MC and not observed in IC. Remodelling of the proximal border, FDPT surface colouration, palmar surface fibrocartilage colouration and proximal border entheseous bone were identified in ND and A‐MC but not in IC. Mid‐ridge synovial fossae and horizontal depressions in the palmar surface were identified in all groups. Histologically palmar fibrocartilage thinning and loss were associated with reduced palmar fibrocartilage cell density and chondrocyte cluster formation. Palmar fibrocartilage fibrillation, palmar cortical bone defects, fibromyxoid stromal change in the medulla, medullary pseudocyst formation and entheseous new bone formation were all seen in ND. The adjacent FDPT showed fibrillation, tag formation and degeneration of the dorsal surface. Necrotic foci were also present within the body of the tendon. Although not always present, medullary bone pseudocysts, separate mineralised foci and most changes on the dorsal surface of the FDPT were specific to ND. Bone histomorphometric parameters were compared among groups. Cross‐sectional area reduced from the sagittal ridge to the medial and lateral margins of each navicular bone. IC navicular bones had a smaller subchondral area, subchondral bone volume and a greater osteoid volume than in the AC, indicating that these differences were age‐related. In ND the medullary area was decreased but the trabecular bone volume increased. The palmar subchondral area was increased but contained bone with an increased porosity and osteoid volume. Changes occurred from the medial to the lateral margins of the bone in horses with ND indicating remodelling of the bony elements throughout the bone in ND. The histological and histomorphometric changes in the navicular bone and palmar fibrocartilage were considered similar of those found in articular hyaline cartilage and subchondral bone in osteoarthritis.

1. This study ascertained how bone of modern meat-type chickens develops under typical commercial conditions and compares development with that in genetic precursor stock. 2. A modern fast-growing selected strain and a slower-growing control strain were used. Birds were weighed weekly. A random sample was taken from each population at a range of ages up to 39 d. 3. A tibiotarsus from each bird was X-rayed and its dimensions and estimated resistance to bending were determined. Cortical bone samples were ashed to measure total mineral, calcium and phosphorus content. Cortical samples were also taken for porosity assessment. 4. As expected, the selected strain grew faster and heavier than the control strain. Despite this, both strains demonstrated similar periods of rapid bone formation (days 4 to 18) and mineralisation (days 4 to 11), and achieved similar estimates of resistance to bending. 5. However, cortical bone of the selected strain was less well mineralised and more porous than that of the control strain and showed a significant increase in the molar Ca:P ratios above the expected range of values during the first 2 to 3 weeks of life. 6. Despite production of bones with the correct dimensions for load support, the relatively poor density and mineral content of bone in the selected strain is likely to reduce effective breaking strength of the tibiotarsus. Possible reasons may be either inadequate dietary supply of Ca and P or impaired utilisation of the minerals due to a rapid growth rate or genetic factors.

The major causes of leg weakness/lameness were investigated in two male commercial broiler flocks. The numbers of dead and lame birds culled from the flocks each day were recorded by the flock managers. Forty-four lame birds and 22 sound birds were examined postmortem during a period of six weeks and the proximal and distal end of each femur, tibiotarsus and tarsometatarsus were examined histologically. Attempts were made to isolate bacteria and viruses from the proximal end of each femur. Blood samples were examined for antibodies to chicken anaemia virus (CAV), infectious bursal disease virus (IBDV) and Mycoplasma species. Bacterial chondronecrosis with osteomyelitis was identified in the proximal end of the femur of eight of the 44 lame birds, and in the proximal end of the tibiotarsus of a further bird (20.4 per cent). Gram-positive bacteria were present in all the lesions. Staphylococcus aureus was recovered from 62.5 per cent of the lesions confirmed by histology. Bacterial chondronecrosis associated with S aureus has thus been identified as an important cause of leg weakness in these commercial broilers. Lesions suggestive of the condition were visible macroscopically in only 11.1 per cent of the cases subsequently diagnosed by histology and bone histology is therefore required before a diagnosis can be excluded. Angular limb deformities (13.6 per cent) and spondylolisthesis (11.4 per cent) were the most common macroscopic lesions identified as causes of lameness. The overall incidence of tibial dyschondroplasia was similar in both the lame and sound broilers, but severe lesions were found only in lame birds (4.5 per cent).

SUMMARYSelection pressure for production traits in modern lines of poultry has placed increasing demands on skeletal integrity. Disruption of the normal process of skeletal growth and homeostasis results in bone diseases that are manifest throughout the modern poultry industry. Bone conditions in poultry can be grouped under three headings based on the age and type of fowls affected, and are indicative of the genetic and production stresses applied to the skeleton. In broilers during growth it is primarily pathologies of the growth plate that lead to most skeletal disorders. In broiler and turkey breeding stock the progressive degeneration of the articular cartilage results in osteoarthrosis, lameness and a consequential loss of reproductive performance. In laying hens bone fragility is most frequently the result of osteoporosis. Before attempting to determine the aetiology of a skeletal disorder an accurate diagnosis must be made. Only then can short-and long-term strategies be developed for the prevention and control of skeletal disorders. Diagnosis requires gross and histological examination, and also dietary, environmental and management analyses. The pathology often reflects lesions initiated when the bird was considerably younger and analyses must extend to assessing the factors prevalent during the initiation of lesions. Current studies are furthering the understanding of the aetiopathogenesis of avian skeletal disorders. For example, structural bone loss at the onset of follicular activity before egg-laying is pivotal to the development of osteoporosis in layers and deficiencies in growth factor expression are integral to the development of tibial dyschondroplasia.

A series of experiments was designed in an attempt to reproduce bacterial chondronecrosis with osteomyelitis in broiler chickens using a natural route of infection. Birds in isolators were exposed to a suspension of Staphylococcus aureus by aerosol or exposed to S. aureus and subsequently inoculated with chicken anaemia virus (CAV) alone, or with CAV and infectious bursal disease virus (IBDV). Subsequently, S. aureus was recovered and bacterial chondronecrosis with osteomyelitis was diagnosed, by histology, in the proximal end of the femur and/or tibiotarsus of lame birds exposed to S. aureus with and without CAV and IBDV infections. Birds fed 60% of the recommended feed intake for the breed developed a lower incidence of S. aureus infection and/or bacterial chondronecrosis (P < 0.05) than birds fed 100% of the recommended intake. A significantly lower incidence of S. aureus was recovered (P < 0.05) in birds simultaneously exposed to S. aureus and inoculated with CAV and IBDV at day 21, than in birds exposed to S. aureus at day 10, and inoculated with CAV and IBDV at day 21. With the exception of birds exposed to S. aureus at 1 day old, a higher incidence of bacterial chondronecrosis was diagnosed in birds exposed to S. aureus and inoculated with CAV and IBDV than in birds exposed to S. aureus alone. It is hypothesised that inoculation with CAV and IBDV at day 21 enhanced the development of bacterial chondronecrosis in birds exposed to S. aureus at day 10 and fed 100% of the recommended feed intake or ad libitum.