The clinical symptoms of acromegaly often manifest as prominent forehead and zygomatic bones. Acromegaly is an abnormal proliferation of skin and bones caused by excessive secretion of growth hormone from the pituitary gland due to hyperplasia or tumors. So, what are the reasons why patients will have prominent forehead and cheekbones? The main effects of GH are to promote the growth of bone tissue, muscle, connective tissue and internal organs, to promote DNA and RNA synthesis, to counteract insulin to promote water and sodium retention, and to stimulate the secretion of some peptides such as growth mediator. GH has both insulin-like and anti-insulin-like effects on glucose metabolism, with the former occurring earlier and the latter later; GH also has a direct effect on pancreatic islet B cells, and about 1/4 of patients can develop diabetes at the same time. Growth interferon (somatomedin, SM) is derived from the liver and can increase cartilage growth through its effect on DNA and RNA protein synthesis. Growth interferon A (SmA) stimulates collagen and non-collagen synthesis, growth interferon C (SmC) stimulates collagen synthesis in osteoblasts, and BGP acts as a result of GH action through SmA. Excess GH accelerates bone formation and maturation and promotes bone growth. Bone remodeling is increased and bone conversion is accelerated. In pituitary dwarfism, the growth and development of bone is halted or delayed due to GH deficiency. In humans, GH increases intestinal calcium absorption, bone formation, and bone mineralization and increases bone mass, while in vitro, it does not directly stimulate bone matrix formation. Growth mediators have growth-promoting effects on various tissues and mediate the effects of GH on bone growth, both in bone and cartilage. GH alters the circadian rhythm variation of serum phosphorus, which increases blood phosphorus, and also increases TRP, which alters the maximum renal phosphorus reabsorption/glomerular filtration rate ratio (TMP/GFR), further increasing blood phosphorus. GH promotes increased TRP and inhibits PTH GH promotes increased TRP and inhibits PTH secretion, resulting in decreased PTH levels, which can also increase blood phosphorus. When patients do not receive enough calcium in the diet, they may have a negative calcium balance, causing osteoporosis, which may change to a positive calcium balance when the dietary calcium intake is increased. GH stimulates subperiosteal bone formation, fibroblasts in the epiphysis differentiate into primitive osteoblasts and promote new bone formation, while the normal epiphysis activity is reactivated, and the cartilage in the epiphyseal plate is actively osteogenic, leading to the proliferation of epiphyseal cartilage. GH can also promote changes in the connective tissue of the joint, with thickening of the joint capsule, fibrosis of the fat pad, and protrusion of fibrous tissue at the junction of bone and cartilage and periosteum. The osteoporosis in acromegaly is different from other osteoporosis in that it is characterized by a decrease in bone mass, but rather by an increase in cortical bone formation with an accelerated calcium conversion rate and an increase in bone mass, which can be characterized by both osteophytes and osteoporosis, or by localized abnormalities such as bone resorption in the dorsal saddle and bone resorption in the saddle base.