Clinical settings in knee osteoarthritis: Pathophysiology guides treatment

[en] Osteoarthritis (OA) is the most common chronic joint disorder and its prevalence increases rapidly during midlife. Complex interactions of genetic alterations, sex hormone deficit, and aging with mechanical factors and systemic inflammation-associated metabolic syndrome lead to joint damage. Thus, the expression of a clinical phenotype in the early stages of OA relies on the main underlying pathway and predominant joint tissue involved at a given time. Moreover, OA often coexists with other morbidities in the same patient, which in turn condition the OA process. In this scenario, an appropriate identification of clinical phenotypes, especially in the early stages of the disease, may optimize the design of individualized treatments in OA. An ESCEO-EUGMS (European Union Geriatric Medicine Society) working group has recently suggested possible patient profiles in OA. Hereby, we propose the existence of 4 clinical phenotypes – biomechanical, osteoporotic, metabolic and inflammatory – whose characterization would help to properly stratify patients with OA in clinical trials or studies. Further research in this field is warranted.

Disciplines :

Rheumatology
Public health, health care sciences & services

Author, co-author :

Herrero-Beaumont, Gabriel

Roman-Blas, Jorge A

Bruyère, Olivier ; Université de Liège > Département des sciences de la santé publique > Santé publique, Epidémiologie et Economie de la santé

Cooper, Cyrus

Kanis, John

Maggi, Stefania

Rizzoli, René

Reginster, Jean-Yves ; Université de Liège > Département des sciences de la santé publique > Santé publique, Epidémiologie et Economie de la santé

Language :

English

Title :

Clinical settings in knee osteoarthritis: Pathophysiology guides treatment

Publication date :

February 2017

Journal title :

Maturitas

ISSN :

0378-5122

eISSN :

1873-4111

Publisher :

Elsevier, Limerick, Ireland

Volume :

Pages :

54-57

Peer reviewed :

Peer Reviewed verified by ORBi

Available on ORBi :

since 13 January 2017

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Bibliography

[1] Cross, M., Smith, E., Hoy, D., Nolte, S., Ackerman, I., Fransen, M., et al. The global burden of hip and knee osteoarthritis: estimates from the global burden of disease 2010 study. Ann. Rheum. Dis. 73 (2014), 1323–1330.
[2] Herrero-Beaumont, G., Roman-Blas, J.A., Castañeda, S., Jimenez, S.A., Primary osteoarthritis no longer primary: three subsets with distinct etiological, clinical, and therapeutic characteristics. Semin. Arthritis Rheum. 39 (2009), 71–80.
[3] Guilak, F., Biomechanical factors in osteoarthritis. Best Pract. Res. Clin. Rheumatol. 25 (2011), 815–823.
[4] Zhuo, Q., Yang, W., Chen, J., Wang, Y., Metabolic syndrome meets osteoarthritis. Nat. Rev. Rheumatol. 8 (2012), 729–737.
[5] Yoshimura, N., Muraki, S., Oka, H., Tanaka, S., Kawaguchi, H., Nakamura, K., et al. Accumulation of metabolic risk factors such as overweight, hypertension, dyslipidaemia, and impaired glucose tolerance raises the risk of occurrence and progression of knee osteoarthritis: a 3-year follow-up of the ROAD study. Osteoarthr. Cartil. 20 (2012), 1217–1226.
[6] Hoeven, T.A., Kavousi, M., Clockaerts, S., Kerkhof, H.J., van Meurs, J.B., Franco, O., et al. Association of atherosclerosis with presence and progression of osteoarthritis: the Rotterdam Study. Ann. Rheum. Dis. 72 (2013), 646–651.
[7] Findlay, D.M., Vascular pathology and osteoarthritis. Rheumatology (Oxf.) 46 (2007), 1763–1768.
[8] Gkretsi, V., Simopoulou, T., Tsezou, A., Lipid metabolism and osteoarthritis: lessons from atherosclerosis. Prog. Lipid Res. 50 (2011), 133–140.
[9] Berenbaum, F., Diabetes-induced osteoarthritis: from a new paradigm to a new phenotype. Ann. Rheum. Dis. 70 (2011), 1354–1356.
[10] Castañeda, S., Roman-Blas, J.A., Largo, R., Herrero-Beaumont, G., Osteoarthritis: a progressive disease with changing phenotypes. Rheumatology (Oxf.) 53 (2014), 1–3.
[11] Bennell, K.L., Bowles, K.A., Wang, Y., Cicuttini, F., Davies-Tuck, M., Hinman, R.S., Higher dynamic medial knee load predicts greater cartilage loss over 12 months in medial knee osteoarthritis. Ann. Rheum. Dis. 70 (2011), 1770–1774.
[12] Teichtahl, A.J., Wang, Y., Heritier, S., Wluka, A.E., Strauss, B.J., Proietto, J., et al. The interaction between physical activity and amount of baseline knee cartilage. Rheumatology 55 (2016), 1277–1284.
[13] Fowler-Brown, A., Kim, D.H., Shi, L., Marcantonio, E., Wee, C.C., Shmerling, R.H., et al. The mediating effect of leptin on the relationship between body weight and knee osteoarthritis in older adults. Arthritis Rheumatol. 67 (2015), 169–175.
[14] Mork, P.J., Holtermann, A., Nilsen, T.I., Effect of body mass index and physical exercise on risk of knee and hip osteoarthritis: longitudinal data from the Norwegian HUNT Study. J. Epidemiol. Commun. Health 66 (2012), 678–683.
[15] Reyes, C., Leyland, K.M., Peat, G., Cooper, C., Arden, N.K., Prieto-Alhambra, D., Association between overweight and obesity and risk of clinically diagnosed knee, hip, and hand osteoarthritis: a population-Based cohort study. Arthritis Rheumatol. 68 (2016), 1869–1875.
[16] Visser, A.W., de Mutsert, R., le Cessie, S., den Heijer, M., Rosendaal, F.R., Kloppenburg, M., for the NEO Study Group, The relative contribution of mechanical stress and systemic processes in different types of osteoarthritis: the NEO study. Ann. Rheum. Dis. 74 (2015), 1842–1847.
[17] Teichtahl, A.J., Wluka, A.E., Tanamas, S.K., Wang, Y., Strauss, B.J., Proietto, J., et al. Weight change and change in tibial cartilage volume and symptoms in obese adults. Ann. Rheum. Dis. 74 (2015), 1024–1029.
[18] Anandacoomarasamy, A., Leibman, S., Smith, G., Caterson, I., Giuffre, B., Fransen, M., et al. Weight loss in obese people has structure-modifying effects on medial but not on lateral knee articular cartilage. Ann. Rheum. Dis. 71 (2012), 26–32.
[19] Teichtahl, A.J., Wluka, A.E., Wang, Y., Strauss, B.J., Proietto, J., Dixon, J.B., et al. The longitudinal relationship between changes in body weight and changes in medial tibial cartilage, and pain among community-based adults with and without meniscal tears. Ann. Rheum. Dis. 73 (2014), 1652–1658.
[20] Roman-Blas, J.A., Castañeda, S., Largo, R., Herrero-Beaumont, G., Osteoarthritis associated with estrogen deficiency. Arthritis Res. Ther., 11, 2009, 241.
[21] Bellido, M., Lugo, L., Roman-Blas, J.A., Castañeda, S., Caeiro, J.R., Dapia, S., et al. Subchondral bone microstructural damage by increased remodelling aggravates experimental osteoarthritis preceded by osteoporosis. Arthritis Res. Ther., 12, 2010, R152.
[22] Sniekers, Y.H., Weinans, H., van Osch, G.J., van Leeuwen, J.P., Oestrogen is important for maintenance of cartilage and subchondral bone in a murine model of knee osteoarthritis. Arthritis Res. Ther., 12, 2010, R182.
[23] Riancho, J.A., García-Ibarbia, C., Gravani, A., Raine, E.V., Rodríguez-Fontenla, C., Soto-Hermida, A., et al. Common variations in estrogen-related genes are associated with severe large-joint osteoarthritis: a multicenter genetic and functional study. Osteoarthr. Cartil. 18 (2010), 927–933.
[24] Lugo, L., Villalvilla, A., Largo, R., Herrero-Beaumont, G., Roman-Blas, J.A., Selective estrogen receptor modulators (SERMs): new alternatives for osteoarthritis. Maturitas 77 (2014), 380–384.
[25] Karsdal, M.A., Bay-Jensen, A.C., Henriksen, K., Christiansen, C., The pathogenesis of osteoarthritis involves bone, cartilage and synovial inflammation: may estrogen be a magic bullet. Menopause Int. 18 (2012), 139–146.
[26] Cirillo, D.J., Wallace, R.B., Wu, L., Yood, R.A., Effect of hormone therapy on risk of hipand knee joint replacement in the Women's Health Initiative. Arthritis Rheum. 54 (2006), 3194–3204.
[27] Prieto-Alhambra, D., Javaid, M.K., Judge, A., Maskell, J., Cooper, C., Arden, N.K., on behalf of the COASt Study Group, Hormone replacement therapy and mid-term implant survival following knee or hip arthroplasty for osteoarthritis: a population-based cohort study. Ann. Rheum. Dis. 74 (2015), 557–563.
[28] Herrero-Beaumont, G., Roman-Blas, J.A., Osteoarthritis: osteoporotic OA: a reasonable target for bone-acting agents. Nat. Rev. Rheumatol. 9 (2013), 448–450.
[29] Marshall, M., Peat, G., Nicholls, E., van der Windt, D., Myers, H., Dziedzic, K., Subsets of symptomatic hand osteoarthritis in community-dwelling older adults in the United Kingdom: prevalence, inter-relationships, risk factor profiles and clinical characteristics at baseline and 3-years. Osteoarthr. Cartil. 21 (2013), 1674–1684.
[30] Jungmann, P.M., Kraus, M.S., Alizai, H., Nardo, L., Baum, T., Nevitt, M.C., et al. Association of metabolic risk factors with cartilage degradation assessed by T2 relaxation time at the knee: data from the osteoarthritis initiative. Arthritis Care Res. (Hoboken) 65 (2013), 1942–1950.
[31] Wen, C.Y., Chen, Y., Tang, H.L., Yan, C.H., Lu, W.W., Chiu, K.Y., Bone loss at subchondral plate in knee osteoarthritis patients with hypertension and type 2 diabetes mellitus. Osteoarthr. Cartil. 21 (2013), 1716–1723.
[32] Stannus, O.P., Cao, Y., Antony, B., Blizzard, L., Cicuttini, F., Jones, G., et al. Cross-sectional and longitudinal associations between circulating leptin and knee cartilage thickness in older adults. Ann. Rheum. Dis. 74 (2015), 82–88.
[33] Karvonen-Gutierrez, C.A., Harlow, S.D., Jacobson, J., Mancuso, P., Jiang, Y., The relationship between longitudinal serum leptin measures and measures of magnetic resonance imaging-assessed knee joint damage in a population of mid-life women. Ann. Rheum. Dis. 73 (2014), 883–889.
[34] Clockaerts, S., Van Osch, G.J., Bastiaansen-Jenniskens, Y.M., Verhaar, J.A., Van Glabbeek, F., Van Meurs, J.B., et al. Statin use is associated with reduced incidence and progression of knee osteoarthritis in the Rotterdam study. Ann. Rheum. Dis. 71 (2012), 642–647.
[35] Scanzello, C.R., Goldring, S.R., The role of synovitis in osteoarthritis pathogenesis. Bone 51 (2012), 249–257.
[36] Sellam, J., Berenbaum, F., The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis. Nat. Rev. Rheumatol. 6 (2010), 625–635.
[37] de Lange-Brokaar, B.J., Ioan-Facsinay, A., Yusuf, E., Visser, A.W., Kroon, H.M., van Osch, G.J., et al. Association of pain in knee osteoarthritis with distinct patterns of synovitis. Arthritis Rheumatol. 67 (2015), 733–740.
[38] Walsh, D.A., Yousef, A., McWilliams, D.F., Hill, R., Hargin, E., Wilson, D., Evaluation of a Photographic Chondropathy Score (PCS) for pathological samples in a study of inflammation in tibiofemoral osteoarthritis. Osteoarthr. Cartil. 17 (2009), 304–312.
[39] Ayral, X., Pickering, E.H., Woodworth, T.G., Mackillop, N., Dougados, M., Synovitis: a potential predictive factor of structural progression of medial tibiofemoral knee osteoarthritis-results of a 1 year longitudinal arthroscopic study in 422 patients. Osteoarthr. Cartil. 13 (2005), 361–367.
[40] Zhang, Y., Nevitt, M., Niu, J., Lewis, C., Torner, J., Guermazi, A., et al. Fluctuation of knee pain and changes in bone marrow lesions, effusions, and synovitis on magnetic resonance imaging. Arthritis Rheum. 63 (2011), 691–699.