Abnormal Bone Metabolism May Be a Primary Causative Factor of Keel Bone Fractures in Laying Hens

SIMPLE SUMMARY: Keel is an essential structural bone, providing anchorage for the attachment of large breast muscles in birds, allowing them to flap wings and provide proper ventilation for their lungs during flight. Previous studies reported that keel bone damage (especially fractures) negatively affects the welfare, health, production performance, eggshell quality, and mobility of laying hens contained in different housing systems. Furthermore, various factors affect keel bone damage, including nutrition, age, housing systems, and strains of laying hens. However, studies on the effects of abnormal bone metabolism and development on keel bone damage in laying hens are limited. Therefore, this study aimed to investigate the impacts of bone metabolism and development status on keel bone damage by determining the levels of serum bone turnover markers in laying hens. The results showed that laying hens with impaired keel bone had significantly altered levels of serum Ca and P metabolism-related and osteoblast and osteoclast activity-related markers compared to those in laying hens with normal keel bone. Thus, these results indicated that abnormal bone metabolism before keel bone damage reflected by varying levels of serum bone turnover markers might be a pivotal factor causing keel bone damage in laying hens. Our results also provide new insights into the occurrence of keel bone damage in laying hens. ABSTRACT: Keel bone damage negatively affects the welfare, production performance, egg quality, and mobility of laying hens. This study aimed to investigate whether abnormal bone metabolism causes keel bone damage in laying hens. Eighty Hy-line Brown laying hens were housed in eight furnished cages with 10 birds per cage and studied from 18 to 29 weeks of age (WOA). Accordingly, keel bone status was assessed at 18, 22, 25, and 29 WOA using the X-ray method, and the serum samples of laying hens with normal keel (NK), deviated keel (DK), and fractured keel (FK) that occurred at 29 WOA were collected across all the time-points. Subsequently, the serum samples were used to measure markers related to the metabolism of Ca and P and activities of osteoblast and osteoclast. The results showed that FK laying hens had lighter bodyweight than NK and DK birds throughout the trial (p < 0.05), while the keel bone length and weight were not different in NK, DK, and FK hens at 29 WOA (p > 0.05). Moreover, bone hematoxylin and eosin (H&E) staining and tartrate-resistant acid phosphatase (TRAP) staining indicated that damaged keel bone had evident pathological changes. In the FK hens, serum P level was reduced but serum 1,25-dihydroxy-vitamin D(3) (1,25-(OH)(2)D(3)) and 25-hydroxyvitamin D(3) (25-OHD(3)) levels were elevated compared to NK hens (p < 0.05). Additionally, DK hens had higher levels of serum 1,25-(OH)(2)D(3), parathyroid hormone (PTH) and calcitonin (CT), and lower level of serum 25-OHD(3) than the NK birds (p < 0.05). Furthermore, serum alkaline phosphatase (ALP), osteocalcin (OC), osteoprotegerin (OPG), TRAP, and corticosterone (CORT) levels were elevated in DK and FK hens compared to NK hens (p < 0.05). The levels of serum Ca, P, PTH, ALP, TRAP, OPG, OC, and CORT in laying hens fluctuated with the age of the birds. Generally, the results of this study indicate that keel bone damage, especially fractures, could be associated with abnormal bone metabolism in laying hens.