Osteonecrosis of the jaw: Difference between revisions

[[Cortical bone]] is well vascularized by the surrounding soft tissues thus less susceptible to ischaemic damage. Cancellous bone, with its mesh like structure and spaces filled with marrow tissue is more susceptible to damage by bone infarcts, leading to [[Hypoxia (medical)|hypoxia]] and premature cell [[apoptosis]].<ref name="Marcus">{{Cite book| author = Marcus R |author2=Feldman D |author3=Kelsey J |title=Osteoporosis |journal=The Journal of Clinical Endocrinology and Metabolism |volume=81 |issue=1 |pages=1–5 |location=San Diego |publisher=Academic Press |year=1996 |isbn=978-0-12-470863-1|pmid=8550734 |doi=10.1210/jcem.81.1.8550734 }}</ref><ref name="Bullough">{{Cite book|author=Bullough PG |title=Orthopaedic pathology |edition=3rd |location=Baltimore |publisher=Wolfe-Mosby |year=1997}}</ref><ref>{{Cite book|author=Kanus JA. |title=Textbook of osteoporosis. |publisher=Blackwell Science Ltd. |location=Osford |year=1996}}</ref><ref>{{Cite book|author=Vigorita VJ. |title=Orthopaedic pathology |location=Philadelphia |publisher=Lippincott Williams & Wilkins |year=1999}}</ref> The mean life-span of osteocytes has been estimated to be 15 years in cancellous bone,<ref>{{cite journal |author=Parfitt AM |title=Osteonal and hemi-osteonal remodeling: the spatial and temporal framework for signal traffic in adult human bone |journal=J. Cell. Biochem. |volume=55 |issue=3 |pages=273–86 |year=1994 |pmid=7962158 |doi=10.1002/jcb.240550303|s2cid=25933384 }}</ref> and 25 years in cortical bone.<ref>{{Cite book| author = Parfin AM |author2=Kleerekoper M |author3=Villanueva AR |chapter=Increased bone age: mechanisms and consequences |title=Osteoporosis |publisher=Osteopress |location=Copenhagen |pages=301–308 |year=1987}}</ref> while the average lifespan of human osteoclasts is about 2 to 6 weeks and the average lifespan of [[osteoblast]]s is approximately 3 months.<ref>{{Cite book| author = Frost HM | publisher = Charles C. Thomas | location = Springfield, IL |title=Bone Remodeling Dynamics |year=1963}}</ref> In healthy bone these cells are constantly replaced by differentiation of bone marrow [[mesenchymal stem cells]] (MSC).<ref>{{cite journal | author = Owen M |author2=Friedenstein AJ |title=Stromal stem cells: marrow- derived osteogenic precursors |journal=Ciba Found Symp |volume=136 |pages=42–60 |year=1988 |pmid=3068016|doi=10.1002/9780470513637.ch4 |series=Novartis Foundation Symposia |isbn=9780470513637 }}</ref> However, in both non-traumatic osteonecrosis and alcohol-induced osteonecrosis of the femoral head, a decrease in the differentiation ability of mesenchymal stem into bone cells has been demonstrated,<ref>{{cite journal | author = Lee JS |author2=Lee JS |author3=Roh HL |author4=Kim CH |author5=Jung JS |author6= Suh KT |title=Alterations in the differentiation ability of mesenchymal stem cells in patients with nontraumatic osteonecrosis of the femoral head: comparative analysis according to the risk factor |journal=J. Orthop. Res. |volume=24 |issue=4 |pages=604–9 |year=2006 |pmid=16514658 |doi=10.1002/jor.20078|doi-access=free }}</ref><ref>{{cite journal | author = Suh KT |author2=Kim SW |author3=Roh HL |author4=Youn MS |author5=Jung JS |title=Decreased osteogenic differentiation of mesenchymal stem cells in alcohol-induced osteonecrosis |journal=Clin. Orthop. Relat. Res. |issue=431 |pages=220–5 |year=2005 |volume=431 |pmid=15685079 |doi=10.1097/01.blo.0000150568.16133.3c|s2cid=24313981 }}</ref> and altered osteoblastic function plays a role in ON of the femoral head.<ref>{{cite journal | author = Gangji V |author2=Hauzeur JP |author3=Schoutens A |author4=Hinsenkamp M |author5=Appelboom T |author6= Egrise D |title=Abnormalities in the replicative capacity of osteoblastic cells in the proximal femur of patients with osteonecrosis of the femoral head |journal=J. Rheumatol. |volume=30 |issue=2 |pages=348–51 |year=2003 |pmid=12563694 }}</ref> If these results are extrapolated to ONJ the altered differentiation potential of bone marrow [[mesenchymal stem cells]] (MSC) combined with the altered osteoblastic activity and premature death of existing bone cells would explain the failed attempts at repair seen in ischaemic-damaged cancellous bone tissue in ONJ.