Boron source–dependent regulation of bone mineralization and osteogenic molecular pathways in broilers with tibial dyschondroplasia

Rapid genetic selection for growth rate and slaughter weight in broilers has been associated with a higher incidence of skeletal disorders, particularly tibial dyschondroplasia (TD), which causes considerable economic losses in poultry production. We investigated the effects of boric acid (BA) and sodium pentaborate pentahydrate (SPP) on growth performance, bone mineralization, tibial histopathology, and osteogenic protein expression in broilers with manganese (Mn) deficiency-induced TD. A total of 360 Ross 308 broiler chicks were used in a 2 × 2 × 3 factorial design with TD status (normal or Mn deficiency–induced TD), boron source (BA or SPP), and supplemental boron level (0, 4.37, and 8.74 mg elemental B/kg diet). Birds were randomly allocated to 12 groups with six replicates of five birds each. Clinical and histopathological findings confirmed TD induction. TD decreased body weight, feed intake, and carcass weight, while increasing feed conversion ratio (p < 0.05). Boron supplementation improved tibial mineral density and content in a dose-dependent manner (p < 0.05). In TD broilers, serum osteocalcin (OCN) concentrations were higher with high-level SPP supplementation than with BA supplementation (p = 0.012). Boron source and level significantly affected serum and bone boron concentrations, bone calcium concentrations (p < 0.05). In TD broilers, tibial osteoprotegerin levels were markedly elevated in the high-level SPP group (p < 0.001), whereas SRY-box transcription factor 9, hypoxia-inducible factor-1α, and tumor necrosis factor-α were reduced (p < 0.05). These findings indicate that SPP exerts regulatory effects on bone metabolism and osteogenic signaling pathways in TD-affected broilers.