Other molecules that play an important role in regulating osteoclast activity include cathepsin K, carbonic anhydrase II, and proteins encoding the proton pump (TCIRG1). Deficiency of these proteins causes osteopetrosis, a congenital disease characterized by increased bone density and defective osteoclast function. In individuals with osteopetrosis, osteoclasts do not function properly, which causes bones to appear dense on X-ray; however, they are actually very fragile and break easily.
The development of a bone is traditionally classified as endochondral or intramembranous.
The distinction between endochondral and intramembranous formation rests on whether a cartilage model serves as the precursor of the bone (endochondral ossification) or whether the bone is formed by a simpler method, without the intervention of a cartilage precursor (intramembranous ossification). The bones of the extremities and those parts of the axial skeleton that bear weight (e.g., vertebrae) develop by endochondral ossification. The flat bones of the skull and face, the mandible, and the clavicle develop by intramembranous ossification.
The existence of two distinct types of ossification does not imply that existing bone is either membrane bone or endochondral bone. These names refer only to the mechanism by which a bone is initially formed. Because of the remodeling that occurs later, the initial bone tissue laid down by endochondral formation or by intramembranous formation is soon replaced. The replacement bone is  established on the preexisting bone by appositional growth and is identical in both cases. Although the long bones are classified as being formed by endochondral formation, their continued growth involves the histogenesis of both endochondral and  FOLDER 8.2
Clinical Correlation: Osteoporosis