The cause of osteolithiasis is unclear, but it may be related to abnormal bone resorption, resulting in excess calcium deposits in the bone with a marble or ivory appearance and increased brittleness. There is a family history of the disease, mostly in the children of consanguineous marriages. It is thought to be hereditary. There are two types of the disease, the light type is dominantly inherited and the heavy type is recessively inherited. Caffey believes that the basic pathological changes of osteomalacia is the formation of bone in the cartilage, the calcified cartilaginous matrix resorption is poor and maintained, the result is that the marrow cavity is reduced, or even occluded, the formation of sclerotic and brittle bone, the bone cortex is also thickened and dense, the cancellous trabeculae are also increased and thickened so that the bone cortex and the cancellous bone is not clearly demarcated. Microscopically, osteoclasts are seen to lose their irregular edges abnormally indicating inactivity. In the skull, it mainly involves the skull base, and in severe cases, the skull cap may also be extensively involved. Pathology: Thickening of bone cortex throughout the body, increased density, lack of osteoclasts, inability to resorb calcified cartilage, osteoid hyperplasia. Genetics: AD, also known as Henck-Assman syndrome. Mostly adult, may be asymptomatic, or invade II, III, or VII cranial nerves. Those with recessive inheritance are severe and invade the bone marrow, so it is also called malignant type.