Simple SummaryGastrointestinal diseases in poultry are more significant because of high economic loss due to production loss, reduced feed efficiency, mortality, compromising bird welfare, and sometimes zoonotic importance. With the removal of antibiotic growth promoters in the diet, gastrointestinal disease incidences have grown in recent years. Gastrointestinal diseases have been shown to affect bone growth negatively; however, possible mechanisms have yet to be confirmed in chickens.AbstractBone serves as a multifunctional organ in avian species, giving structural integrity to the body, aiding locomotion and flight, regulating mineral homeostasis, and supplementing calcium for eggshell formation. Furthermore, immune cells originate and reside in the bone marrow, sharing a milieu with bone cells, indicating a potential interaction in functions. In avian species, the prevalence of gastrointestinal diseases can alter the growth and the immune response, which costs a great fortune to the poultry industry. Previous studies have shown that coccidiosis and necrotic enteritis can dramatically reduce bone quality as well. However, possible mechanisms on how bone quality is influenced by these disease conditions have not yet been completely understood, other than the reduced feed intake. On the other hand, several mediators of the immune response, such as chemokines and cytokines, play a vital role in the differentiation and activation of osteoclasts responsible for bone resorption and osteoblasts for bone formation. In the case ofEimeriaspp./Clostridium perfringenscoinfection, these mediators are upregulated. One possible mechanism for accelerated bone loss after gastrointestinal illnesses might be immune-mediated osteoclastogenesis via cytokines-RANKL-mediated pathways. This review article thus focuses on osteoimmunological pathways and the interaction between host immune responses and bone biology in gastrointestinal diseases like coccidiosis and necrotic enteritis affecting skeletal health.