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Very often, people need a surgery for lengthening, shortertening bones.

Surgeons can perform osteotomy and place bone fragments in corrent position, or can place a distractor for further steps. Most resistance in bones located in outer cortex, sometimes surgeon can remove this cortex(corticotomy). Bone rigid because of hydroxyapatite crystals,demineralized bone matrix have diminished resistance for deformation.

We have a chemical compouds such as EDTA,EGTA. It's chelating agents, that can destroy hydroxyapatite by chelating calcium. It's low mutagenic, low cytotoxic.

Why we can't perform "chemical corticotomy" by subperiosteally injecting EDTA, or it can be by sustained-release drug delivery(hydrogels,polymers)? Can we inject EDTA, wait for demineralization, and after place distractor on bone?

neron neronium
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  • Interesting premise. Welcome. This site isn't well suited to "what if we..." or "why don't we do it this way?" type questions for several reasons, mostly due to the fact that most such questions provide limited background knowledge/research, and also the limited number of expert involvement to make such discussions feasible and not invite wild speculation. But you provided good background, which we appreciate. I am curious, how would you propose limiting the chelation to only the area of bone to be removed? That still involves surgical extraction, so is it worth doing it? – DoctorWhom Jun 18 '19 at 18:27
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    If used to lengthen bone, how do we re-mineralize the bone after the distractor? The biggest challenge facing your proposal is the fact that increasing bone density e.g. re-mineralization is currently a difficult task. Bisphosphonates and other agents are systemic and can't be applied to a single site, as far as my knowledge carries me. (If you found a way to do THAT, it would be a great advancement!) Therefore, unless all the weakened bone is removed, you leave the patient with osteomalacia, with fracture risk etc likely worse than the condition for which the leg was lengthened. – DoctorWhom Jun 18 '19 at 18:27
  • Thank you for reply. First of all, about limiting bone area: after injection EDTA molecules cleaned by diffussion between extracellular fluid and blood vessel, and EDTA do not spread too far after injection. Example: subperiosteal local anaesthetic inflitration. – neron neronium Jun 18 '19 at 19:17
  • Re-mineralization is not a problem in healthy bone, if someone has osteomalacia, hyperparathyroidism, fracture, or another similar disease, after time bone re-mineralize without addional treatment. – neron neronium Jun 18 '19 at 19:20
  • Interesting, I had the impression that chemical demineralization creates a trabeculation structure that resists complete remineralization, but I must admit my knowledge in the further details is somewhat limited. – DoctorWhom Jun 18 '19 at 19:27
  • In bone sample it can, but in the body osteoblasts and osteoclasts constantly remodeling our bones, osteoblasts expressing alkaline phosphotase that produce mineralization... In my opinion the biggest problems are 1)EDTA is slow, and we need many injections to demineralize bone, to fix this issue we can create EDTA hydrogel-based sustained-release gel. 2) after bone demineralize,we can do traction, but without correct tractiob protocol, we can easily fracture bone (demineralized matrix have diminished tensile strength, but increased maximum tensile strain) – neron neronium Jun 18 '19 at 19:37
  • Decalcification of calcific shoulder tendinitis using EDTA: https://www.researchgate.net/publication/23714170_Effectiveness_of_Treatment_of_Calcific_Tendinitis_of_the_Shoulder_by_Disodium_EDTA – neron neronium Jun 18 '19 at 19:39

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