The specific cause of<unk>  remains unknown. Bone mass and strength are obtained and maintained through a process of bone destruction and replacement that occurs at the cellular level throughout a person's life. Cells called osteoclasts secrete enzymes that dissolve old bone, allowing another type of cells called osteoblasts to form new bone. Except in growing bone, the rate of breakdown equals the rate of building, thereby maintaining bone mass. In<unk> , that process is disrupted.<unk>  and Stout found that vascular anomalies always occupied space that normally would be filled with new bone and speculated that the presence of angiomatosis may lead to chemical changes in the bone.<unk>  and others speculated that such a change in the bone chemistry might cause an imbalance in the rate of osteoclast to osteoblast activity such that more bone is dissolved than is replaced. Beginning in the 1990s, elevated levels of a protein called interleukin-6 (IL-6) being detected in people with the disease were reported, leading some to suggest that increased levels of IL-6 and vascular endothelial growth factor (VEGF) may contribute to the chemical changes<unk>  and others believed were the cause of this type of osteolysis. In 1999, Möller and colleagues concluded, "The<unk> -Stout syndrome may be, essentially, a monocentric bone disease with a focally increased bone resorption due to an increased number of paracrine – or autocrine – stimulated hyperactive osteoclasts. The resorbed bone is replaced by a markedly vascularized fibrous tissue. The apparent contradiction concerning the presence or absence or the number of osteoclasts, may be explained by the different phases of the syndrome." They further stated that their histopathological study provided good evidence that osteolytic changes seen in<unk>  are the result of hyperactive osteoclastic bone. However, others have concluded that lymphangiomatosis and<unk>  should be considered as a spectrum of disease rather than separate diseases. While a consensus exists that<unk> 's is caused by deranged osteoclastic activity, no conclusive evidence has been found as to what causes this behavior to begin.
Gorham's disease
Darier's disease
Chandler's disease
Texier's disease
Camisa disease
Milroy's disease
Minor's disease
Tornwaldt's disease