Me: I got an email recently from Tyler to do a little research on a condition called Multiple Exotoses to see whether it might have any connection with possible height increase. Wikipedia is always the first link that appears. however, the term that is most cited is NOT multiple exoduses but “hereditary multiple exoduses”.

From this link here…

“Extosis – An exostosis is a bone growth that is abnormal or different from the underlying architecture of the bone. These “abnormal growths” are not cancer, They are benign. Sometimes doctors refer to exostoses as “tumors” which like exostose is a general term meaning abnormal growth.”

It seems that Hereditary Multiple Exotoses (aka HME or MHE) is where you get multiple bone spurs and lumps that appear on the bone.  However, for the Hereditary type, HME, this condition only affects children. Hence the hereditary part. From the wikipedia article on HME (HERE)…

“It is characterized by the growth of cartilage-capped benign bone tumours around areas of active bone growth, particularly the metaphysis of the long bones. HME can lead to the shortening and bowing of bones; affected individuals often have a short stature….A person with HME has an increased risk of developing a rare form of bone cancer called chondrosarcoma as an adult. Problems may be had in later life and these could include weak bones and nerve damage.”

It seems the condition can not be cured and that the two most common treatments are surgical methods to  remove the bone spurs/lumps but the osteosarcoma just reappears in the same place later on. The big thing seems to be that the spurs causes a lot of pain. The condition is autosomally dominant and hereditary with a 96% change of a person expressing it if they have the dominant gene. It will be transferred to the children of parent with it. It can also just come about spontaneously. Wikipedia says that “Since the HME genes are involved in the synthesis of a glycan (heparan sulfate), HME may be considered a congenital disorder of glycosylation”. We know that Heparan sulfate is a member of the glycosaminoglycan family of carbohydrates or a proteoglycan. The exact mechanism for how a mutation in the 3 genes associated with HME actually affects bone growth is not known yet. They are…

• EXT1 which maps to chromosome 8q24.1,  EXT2 which maps to 11p13,  EXT3 which maps to the short arm of Chromosome 19

From the genetics home reference website on the National Institute of Health website located HERE the thing they say about HME is that it only is expressed in children, and by the time the kid is 12, they most likely would have expressed the exoduses. However, when they turn into adults and they stop growing in size, i.e.. their growth plates have fused, the bone growths stop. The thing about multiple exoduses is that when a person gets the disorder, it doesn’t increase bone length but disrupts the growth process leading to short stature, stunting growth ,and limb curvature. The condition is usually non-cancerous. It seems to be a rather rare condition.

From WheelersOnline.com…

It is an osteochondroma that results from a dysplasia of peripheral growth plate. Dysplasia is a term used in pathology to refer to an abnormality of development. This generally consists of an expansion of immature cells, with a corresponding decrease in the number and location of mature cells. It also seems this disorder can be diagnosed rather early, usually around 3.  from the source…

“- cartilaginous exostoses arise from metaphyses, point away from epiphysis, and appear to extend down diaphysis during growth;”

Again it is stated that they increase in size & number w/ growth, but may become latent at maturity. The disorder really only affects people with their growth plates open, children. If the person has stopped increasing in height, they have become the very small minority of people where the exotoses has turned into Chondrosarcoma.

The link between this disorder and longitudinal growth seems to be from the study found below…

EXT1 regulates chondrocyte proliferation and differentiation during endochondral bone development.