title: [Bone resorption in posttraumatic dystrophy. Root cause analysis based on the literature].
abstract: BACKGROUND
  In posttraumatic dystrophy the resorption of cancellous bone remains an unsolved phenomenon.
  
  
  OBJECTIVE
  The possible effects of arteriovenous (av) anastomoses, hypoxia and acidosis in posttraumatic dystrophy on cancellous bone structures should be elucidated.
  
  
  METHODS
  In posttraumatic dystrophy of the hand after distal radius fracture, hand fractures and elective hand surgery [20] the results suggest that persistent av anastomoses could be the reason for this syndrome. Possible pathways for the occurrence of cancellous bone resorption are discussed in context with the literature.
  
  
  CONCLUSIONS
  Intraosseous av anastomoses with acidosis and hypoxia of the tissues are probably responsible for the excessive activity of osteoclasts in acute posttraumatic dystrophy. Even enhancements in the late static phase of the three phase bone scan (TPBS) are in agreement with this hypothesis. In cancellous bone these enhancements are induced by the bone seeking tracers. The nomenclature for these tracer molecules is in line with the recommendations of International Union of Pure and Applied Chemistry (IUPAC) as methylene bisphosphonate and hydroxymethylene bisphosphonate. From this, therapeutic recommendations for posttraumatic dystrophy can be derived. The term diphosphonates should be changed to bisphosphonates.
authors.affiliation: Klinik für Unfall-, Hand-, Plastische- und Wiederherstellungschirurgie, Universitätsklinikum Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Deutschland, alexander.scola@uniklinik-ulm.de.
authors.forename: A
authors.initials: A
authors.lastname: Scola
authors.forename: E
authors.initials: E
authors.lastname: Scola
mesh_terms: D001862:Bone Resorption / Q000209:etiology* / Q000503:physiopathology*; D001842:Bone and Bones / Q000503:physiopathology*; D019317:Evidence-Based Medicine; D006801:Humans; D008954:Models, Biological; D012019:Reflex Sympathetic Dystrophy / Q000150:complications* / Q000503:physiopathology*; D014947:Wounds and Injuries / Q000150:complications* / Q000503:physiopathology*