In Pteropus spp., metabolic bone disease has been consistently associated with fruit-based diets that are deficient in calcium, vitamin D precursors, and protein, as well as limited ultraviolet B (UVB) exposure, as reported in zoological surveys and clinical observations. Comparative mammalian physiology suggests that dysregulation of the endocrine axis involving parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), calcitonin, and calcitriol may contribute to disease development, although direct species-specific endocrine data in flying foxes remain scarce. This narrative review synthesizes current knowledge from published zoological reports, clinical observations, and comparative mammalian physiology regarding the etiology, pathophysiology, and clinical expression of metabolic bone disease in captive flying foxes. Much of the available evidence is derived from juvenile Pteropus vampyrus, and its applicability to other Pteropus species remains to be fully established. The limited availability and consistency of existing data, together with the scarcity of controlled experimental and longitudinal studies, necessarily constrain the conclusions that can be drawn. Nevertheless, this review highlights key nutritional and environmental risk factors and summarizes evidence-informed preventive management strategies to improve skeletal health and welfare in managed Pteropus populations.
Faim et al. (Wed,) studied this question.