<unk> s are long and slender, pedunculated on a stalk often taking the shape of a cauliflower. The cartilage cap is covered by fibrous perichondrium and continues with the periosteum of the underlying bone. The cartilage cap is less than 2 cm thick and the thickness decreases with age. A cap more than 2 cm thick, indicates malignant transformation of a tumor. The cartilage cap merges with the epiphyseal area of the long bones called spongiosa. In the spongiosa, the chondrocytes are arranged in accordance with the epiphyseal growth plate. The spongiosa of the stalk continues with the underlying cancellous bone. Fractures within the stalk causes fibroblastic proliferation and formation of a new bone. Development of bursa takes place over the<unk> , which is attached to the perichondrium of the cap. Inflammation of the bone is indicated by the bursal wall lined by the synovium. As a result, patients may have swelling for years related to the location and site of the lesion indicative of mechanical obstruction, nerve impingement, pseudoaneurysm of the overlying vessel, fracture at the stalk of the lesion, or formation of bursa over the<unk> . Heparan sulphate (HS) are glycosaminoglycans which are involved in the formation of proteoglycans. The biosynthesis of HS takes place in the Golgi apparatus and endoplasmic reticulum, where glycosaminoglycans chains are maintained by type II glycosyltransferases encoded by EXOSTOSIN genes EXT1 and EXT2. Decreased levels of HS leads to mutations in EXT1 or EXT2 causing skeletal abnormality. The underlying mechanism for solitary and multiple<unk> s have been associated with genetic alterations in EXT1 or EXT2 genes located on chromosomes 8 and 11. Approximately 65% of<unk> s arise in the EXT1 gene loci on chromosome 8 and 35% arise in EXT2 gene loci on chromosome 11. About 70–75% of multiple<unk> s are caused by point mutations, often involving deletion of single or multiple axons as found in 10% of all hereditary cases. In about 10–15% of all cases no genomic alterations are detected. The mechanism behind the formation of multiple<unk>  is large genomic deletions of EXT1 and EXT2 genes. The identified mechanism behind solitary<unk> s is the homozygous deletions of the EXT1 gene. However, the exact cause of<unk>  is unknown. Additionally, the molecular basis of genetics and clinical variability of multiple<unk>  as well as the underlying causes for the malignant transformation and the onset of<unk>  in EXT negative patients is also currently unknown.
Osteochondroma
Osteochondrosis
Bone cyst
Osteoma
Osteoblastoma
Osteoid osteoma
Osteosarcoma
Synovial sarcoma