Vascular pathology and osteoarthritis

被引:202
作者
Findlay, D. M.
机构
[1] Univ Adelaide, Discipline Orthopaed & Trauma, Adelaide, SA 5000, Australia
[2] Hanson Inst, Adelaide, SA, Australia
基金
英国医学研究理事会;
关键词
osteoarthritis; blood vessels; subchondral bone; venous stasis; hypertension; hypercoagulability; hypoxia; osteocyte viability; osteoclast;
D O I
10.1093/rheumatology/kem191
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
There is mounting evidence that vascular pathology plays a role in the initiation and/or progression of the major disease of joints: osteoarthritis (OA). Potential mechanisms are: episodically reduced blood flow through the small vessels in the subchondral bone at the ends of long bones, and related to this, reduced interstitial fluid flow in subchondral bone. Blood flow may be reduced by venous occlusion and stasis or by the development of microemboli in the subchondral vessels. There are several likely effects of subchondral ischaemia: the first of these is compromised nutrient and gas exchange into the articular cartilage, a potential initiator of degradative changes in the cartilage. The second is apoptosis of osteocytes in regions of the subchondral bone, which would initiate osteoclastic resorption of that bone and at least temporarily reduce the bony support for the overlying cartilage. It may be important to recognize these potential aetiological factors in order to develop more effective treatments to inhibit the progression of OA.
引用
收藏
页码:1763 / 1768
页数:6
相关论文
共 86 条
  • [1] Osteocyte apoptosis is induced by weightlessness in mice and precedes osteoclast recruitment and bone loss
    Aguirre, JI
    Plotkin, LI
    Stewart, SA
    Weinstein, RS
    Parfitt, AM
    Manolagas, SC
    Bellido, T
    [J]. JOURNAL OF BONE AND MINERAL RESEARCH, 2006, 21 (04) : 605 - 615
  • [2] Hypoxia is a major stimulator of osteoclast formation and bone resorption
    Arnett, TR
    Gibbons, DC
    Utting, JC
    Orriss, IR
    Hoebertz, A
    Rosendaal, M
    Meghji, S
    [J]. JOURNAL OF CELLULAR PHYSIOLOGY, 2003, 196 (01) : 2 - 8
  • [3] INTRAOSSEOUS HYPERTENSION AND PAIN IN KNEE
    ARNOLDI, CC
    LEMPERG, RK
    LINDERHOLM, H
    [J]. JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME, 1975, 57 (03): : 360 - 363
  • [4] Arnoldi CC, 1984, BONE CIRCULATION, P213
  • [5] Shear stress inhibits while disuse promotes osteocyte apoptosis
    Bakker, A
    Klein-Nulend, J
    Burger, E
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2004, 320 (04) : 1163 - 1168
  • [6] Relationships between trabecular bone remodeling and bone vascularization: A quantitative study
    Barou, O
    Mekraldi, S
    Vico, L
    Boivin, G
    Alexandre, C
    Lafage-Proust, MH
    [J]. BONE, 2002, 30 (04) : 604 - 612
  • [7] Effects of calcitonin on subchondral trabecular bone changes and on osteoarthritic cartilage lesions after acute anterior cruciate ligament deficiency
    Behets, C
    Williams, JM
    Chappard, D
    Devogelaer, JP
    Manicourt, DH
    [J]. JOURNAL OF BONE AND MINERAL RESEARCH, 2004, 19 (11) : 1821 - 1826
  • [8] Biochemical markers of bone metabolism in bone marrow edema syndrome of the hip
    Berger, CE
    Kröner, AH
    Minai-Pour, MB
    Ogris, E
    Engel, A
    [J]. BONE, 2003, 33 (03) : 346 - 351
  • [9] Evidence for increased bone resorption in patients with progressive knee osteoarthritis - Longitudinal results from the Chingford study
    Bettica, P
    Cline, G
    Hart, DJ
    Meyer, J
    Spector, TD
    [J]. ARTHRITIS AND RHEUMATISM, 2002, 46 (12): : 3178 - 3184
  • [10] Vascular biology and the skeleton
    Brandi, ML
    Collin-Osdoby, P
    [J]. JOURNAL OF BONE AND MINERAL RESEARCH, 2006, 21 (02) : 183 - 192