Volume 14 Supplement 2

Proceedings of Osteorheumatology 2011: International Congress on Bone Involvement in Arthritis

Open Access

Clinical significance of bone changes in osteoarthritis

  • Tuhina Neogi1
Arthritis Research & Therapy201214(Suppl 2):A3

DOI: 10.1186/ar3710

Published: 8 March 2012

Knee OA is thought to be a largely mechanically-driven disease. Pertinent to this, bone is a dynamic tissue that adapts to loads by remodeling to meet its mechanical demands (Wolff's Law) [1, 2]. As such, it is not surprising that bone changes, such as increased tibial plateau area and bone turnover, occur early in OA [3, 4]. Recently, MRI-based 3D bone shape has been shown to track concurrently with OA onset, and to predict incidence of radiographic knee OA 12 months before its onset [5]. Further, in radiographically normal tibiofemoral knee joints, subchondral bone changes, such as bone marrow lesions (BMLs) on MRIs, are common.

Although MRIs allow direct visualization and morphologic evaluation of joint tissues not otherwise discernible on x-ray, their specific pathologies need to be examined by direct evaluation to gain further pathophysiologic insight. BMLs adjacent to the subchondral plate have been shown to have increased bone volume fraction and increased trabecular thickness, but reduced tissue mineral density (i.e., hypomineralized) [6], consistent with OA being associated with increased bone turnover. BMLs may render these areas mechanically compromised and susceptible to attrition. Indeed, BMLs are strongly associated with occurrence of subchondral bone attrition (SBA) [7]. Both subchondral bone abnormalities are associated with cartilage loss as well [8, 9]. In keeping with knee OA being mechanically-driven, meniscal pathology, often the result of injury, is associated with new and enlarging BMLs [10]. Further, malalignment is associated with both BMLs and SBA [11, 12].

The contributions of these structural abnormalities to the clinical manifestations of knee OA are becoming better understood. While it is widely thought that there is a structure-symptom discordance in knee OA, such observations do not take into account all of the potential factors that can contribute to between-person differences in the pain experience [13]. Recent work that used novel methodology to overcome this problem has demonstrated that pain fluctuation is associated with changes in BMLs, as well as synovitis and effusion [14]. SBA has also been associated with knee pain [15], but the relationship of osteophytes to pain has been conflicting. A challenge that remains in studying the specific contribution of pathologic features of OA to pain is the co-existence of multiple MRI abnormalities, making it difficult to identify individual pathologic features' effects.

Understanding the pathophysiologic sequences and consequences of OA pathology will guide rational therapeutic targeting. Importantly, rational treatment targets also require understanding what particular structures contribute to pain as pain is the reason patients seek medical care.

Authors’ Affiliations

(1)
Section of Clinical Epidemiology Research and Training Unit, and Rheumatology, Department of Medicine, Boston University School of Medicine

References

  1. Chen JH, Liu C, You L, Simmons CA: Boning up on Wolff's Law: mechanical regulation of the cells that make and maintain bone. J Biomech. 2010, 43: 108-118. 10.1016/j.jbiomech.2009.09.016.View ArticlePubMedGoogle Scholar
  2. Goldring SR: The role of bone in osteoarthritis pathogenesis. Rheum Dis Clin North Am. 2008, 34: 561-571. 10.1016/j.rdc.2008.07.001.View ArticlePubMedGoogle Scholar
  3. Burr DB: Subchondral bone in the pathogenesis of osteoarthritis. Mechanical aspects. Osteoarthritis. Edited by: Brandt KD, Doherty M, Lohmander LS. 2003, Oxford: Oxford University Press, 125-133. 2Google Scholar
  4. Radin EL, Rose RM: Role of subchondral bone in the initiation and progression of cartilage damage. Clin Orthop Relat Res. 1986, 34-40.Google Scholar
  5. Neogi T, Bowes M, Niu J, De Souza K, Goggins J, Zhang Y, Felson D: MRI-based 3D bone shape predicts incident knee OA 12 months prior to its onset. Osteoarthritis Cartilage. 2011, 19 (Suppl 1): S51-S52.View ArticleGoogle Scholar
  6. Hunter DJ, Gerstenfeld L, Bishop G, Davis AD, Mason ZD, Einhorn TA, Maciewicz RA, Newham P, Foster M, Jackson S, Morgan EF: Bone marrow lesions from osteoarthritis knees are characterized by sclerotic bone that is less well mineralized. Arthritis Res Ther. 2009, 11: R11-10.1186/ar2601.PubMed CentralView ArticlePubMedGoogle Scholar
  7. Roemer FW, Neogi T, Nevitt MC, Felson DT, Zhu Y, Zhang Y, Lynch JA, Javaid MK, Crema MD, Torner J, Lewis CE, Guermazi A: Subchondral bone marrow lesions are highly associated with, and predict subchondral bone attrition longitudinally: the MOST study. Osteoarthritis Cartilage. 2010, 18: 47-53. 10.1016/j.joca.2009.08.018.PubMed CentralView ArticlePubMedGoogle Scholar
  8. Neogi T, Felson D, Niu J, Lynch J, Nevitt M, Guermazi A, Roemer F, Lewis CE, Wallace B, Zhang Y: Cartilage loss occurs in the same subregions as subchondral bone attrition: a within-knee subregion-matched approach from the Multicenter Osteoarthritis Study. Arthritis Rheum. 2009, 61: 1539-1544. 10.1002/art.24824.PubMed CentralView ArticlePubMedGoogle Scholar
  9. Hunter DJ, Zhang Y, Niu J, Goggins J, Amin S, LaValley MP, Guermazi A, Genant H, Gale D, Felson DT: Increase in bone marrow lesions associated with cartilage loss: a longitudinal magnetic resonance imaging study of knee osteoarthritis. Arthritis Rheum. 2006, 54: 1529-1535. 10.1002/art.21789.View ArticlePubMedGoogle Scholar
  10. Englund M, Guermazi A, Roemer FW, Yang M, Zhang Y, Nevitt MC, Lynch JA, Lewis CE, Torner J, Felson DT: Meniscal pathology on MRI increases the risk for both incident and enlarging subchondral bone marrow lesions of the knee: the MOST Study. Ann Rheum Dis. 2010, 69: 1796-1802. 10.1136/ard.2009.121681.PubMed CentralView ArticlePubMedGoogle Scholar
  11. Neogi T, Nevitt M, Niu J, Sharma L, Roemer F, Guermazi A, Lewis CE, Torner J, Javaid K, Felson D: Subchondral bone attrition may be a reflection of compartment-specific mechanical load: the MOST Study. Ann Rheum Dis. 2010, 69: 841-844. 10.1136/ard.2009.110114.PubMed CentralView ArticlePubMedGoogle Scholar
  12. Felson DT, McLaughlin S, Goggins J, LaValley MP, Gale ME, Totterman S, Li W, Hill C, Gale D: Bone marrow edema and its relation to progression of knee osteoarthritis. Ann Intern Med. 2003, 139: 330-336.View ArticlePubMedGoogle Scholar
  13. Neogi T, Felson D, Niu J, Nevitt M, Lewis CE, Aliabadi P, Sack B, Torner J, Bradley L, Zhang Y: Association between radiographic features of knee osteoarthritis and pain: results from two cohort studies. BMJ. 2009, 339: b2844-10.1136/bmj.b2844.PubMed CentralView ArticlePubMedGoogle Scholar
  14. Zhang Y, Nevitt M, Niu J, Lewis C, Torner J, Guermazi A, Roemer F, McCulloch C, Felson D: Reversible MRI features and fluctuation of knee pain severity: the MOST Study. Arthritis Rheum. 2008, 58: S234-Google Scholar
  15. Torres L, Dunlop DD, Peterfy C, Guermazi A, Prasad P, Hayes KW, Song J, Cahue S, Chang A, Marshall M, Sharma L: The relationship between specific tissue lesions and pain severity in persons with knee osteoarthritis. Osteoarthritis Cartilage. 2006, 14: 1033-1040. 10.1016/j.joca.2006.03.015.View ArticlePubMedGoogle Scholar

Copyright

© Neogi; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Advertisement