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Wiener Medizinische Wochenschrift

, Volume 163, Issue 9–10, pp 212–219 | Cite as

Osteoarthritis: histology and pathogenesis

  • Irene SulzbacherEmail author
main topic

Summary

Osteoarthritis is the most common joint disease, affecting over 60 % of the elderly population, leading to incapacity of movement. The primary form is usually oligoarticular. In case of an underlying systemic disease or local injury, the cartilage destruction is considered as secondary osteoarthritis. The pathogenesis of primary osteoarthritis suggests an intrinsic disease of cartilage in which biochemical and metabolic alterations result in its breakdown. Within the last decades, different models were established concentrating on joint structures such as bones or ligaments. Changes of the subchondral bone were found to precede cartilage damage, suggesting a primary alteration of the subchondral region. Other studies concentrated on the metabolic activity of chondrocytes in healthy cartilage of patients with osteoarthritis. The precise event that leads to these changes is still not clear. This review concentrates on the histological features in the course of the disease and provides a summary on different pathogenetic risk factors.

Keywords

Joint Osteoarthritis Histology Pathogenesis 

Arthrose: Histologie und Pathogenese

Zusammenfassung

Die Arthrosis deformans ist die häufigste Gelenkserkrankung und betrifft über 60 % der älteren Population. Die Erkrankung ist durch fortschreitenden Knorpelverust gekennzeichnet und führt zu einer limitierterten Bewegungsfreiheit. In den meisten Fällen beginnt der Krankheitsverlauf spontan ohne ersichtlichen Grund. Diese primäre Form manifestiert sich oft oligoartikulär und betrifft vor allem die Hüfte, das Knie, die Halswirbelsäule, die interphalangealen Gelenke der Finger oder die tarsometatarsalen Gelenke. Bei einer zugrunde liegenden systemischen Erkrankung oder lokal destruierenden Faktoren ist der Knorpelabbau als sekundäre Arthrose zu bezeichnen. Die Pathogenese der primären Arthrose basiert auf einer intrinsischen Erkrankung des Knorpels, bei der biochemische und metabolische Veränderungen zu dessen Zusammenbruch führen. In den letzten Jahrzehnten wurden auch pathogenetische Modelle entworfen, die andere Gelenksanteile wie Knochen oder den Bandapparat in den Mittelpunkt stellen. Veränderungen des subchondralen Knochens, die dem Knorpelabbau voran gehen, lenkten die Aufmerksamkeit auf die subchondrale Region als Ort des primären Geschehens. Weitere Untersuchungen konzentrierten sich auf die metabolische Aktivität der Chondrozyten im unveränderten Knorpelgewebe von Arthrosepatienten. Der ausschlaggebende Faktor für den Krankheitsbeginn ist jedoch immer noch unklar. Dieser Übersichtsartikel beschreibt die morphologischen Veränderungen in Abhängigkeit des Krankheitsstadiums und gibt einen Einblick über verschiedene pathogenetische Risikofaktoren.

Schlüsselwörter

Gelenk Arthrose Histologie Pathogenese 

Notes

Conflict of interest

The author declares that there is no conflict of interest.

References

  1. 1.
    Klein MJ, Bonar SF, Freemont T, et al. Biology of joints. In: Donald West King, editor. Atlas of non tumour pathology, non neoplastic diseases of bones and joints. Fascicle 9. Maryland: ARP Press; 2011. pp. 545–76.Google Scholar
  2. 2.
    Griffin TM, Guilak F. The role of mechanical loading in the onset and progression of osteoarthritis. Exerc Sport Sci Rev. 2005;33(4):195–200.PubMedCrossRefGoogle Scholar
  3. 3.
    Otte P. Die konservative Behandlung der Hüft-und Kniearthrose und ihre Gefahren. Dtsch Med Jahresschr. 1969;20:604–9.Google Scholar
  4. 4.
    Mankin HJ, Dorfman H, Lippiello L, et al. Biochemical and metabolic abnormalities in articular cartilage from osteoarthritis human hips. II. Correlation of morphology with biochemical and metabolic data. J Bone Joint Surg Am. 1971;53:523–37.PubMedGoogle Scholar
  5. 5.
    Pelletier JP, Martell-Pelletier J, Abramson SB. Osteoarthritis, an Inflammatory Disease: potential implication for the selection of new therapeutic targets. Arthritis Rheum. 2001;44:1237–47.PubMedCrossRefGoogle Scholar
  6. 6.
    Goldring MB. Anticytokine therapy for osteoarthritis. Expert Opin Biol Ther. 2001;1:817–29.PubMedCrossRefGoogle Scholar
  7. 7.
    Goldberg SH, Von Feldt JM, Lonner HJ. Pharmacologic therapy for osteoarthritis. Am J Orthop. 2002;31:673–80.PubMedGoogle Scholar
  8. 8.
    Goggs R, Carter SD, Schulze-Tanzil G, et al. Apoptosis and the loss of chondrocyte survival signals contribute to articular cartilage degradation in osteoarthritis. Vet J. 2003;166:140–58.PubMedCrossRefGoogle Scholar
  9. 9.
    Feng L, Balakir R, Precht P, et al. Bcl-2 regulates chondrocyte morphology and aggrecan gene expression independent of caspade activation and full apoptosis. J Cell Biochem. 1999;74:576–86.PubMedCrossRefGoogle Scholar
  10. 10.
    Denko CW, Malemud CJ. Metabolic disturbances and synovial joint responses in osteoarthritis. Front Biosci. 1999;4:D686–93.PubMedGoogle Scholar
  11. 11.
    Adatia A, Rainsford KD, Kean WF. Osteoarthritis of the knee and hip. Part I: aetiology and pathogenesis as a basis for pharmacotherapy. J Pharm Pharmacol. 2012;64:617–25.PubMedCrossRefGoogle Scholar
  12. 12.
    Hutton WC, Higgs ER, Jackson PC, et al. 99mTcHMDP bone scanning in generalised nodal osteoarthritis. II. The four hour bone scan image predicts radiographic change. Ann Rheum Dis. 1986;45:622–6.Google Scholar
  13. 13.
    Dieppe P, Cushnaghan J, Young P, et al. Prediction of the progression of joint space narrowing in osteoarthritis of the knee by bone scintigraphy. Ann Rheum Dis. 1993;52:557–63.PubMedCrossRefGoogle Scholar
  14. 14.
    Petersson IF, Boegard T, Svensson B, et al. Changes in cartilage and bone metabolism identified by serum markers in early osteoarthritis of the knee joint. Br J Rheumatol. 1998;37:46–50PubMedCrossRefGoogle Scholar
  15. 15.
    Mrosek EH, Lahm A, Erggelet C, et al. Subchondral bone trauma causes cartilage matrix degeneration: an immunohistochemical analysis in a canine model. Osteoarthritis Cartilage. 2006;14:171–8PubMedCrossRefGoogle Scholar
  16. 16.
    Muraoka T, Hagino H, Okano T, et al. Role of subchondral bone in osteoarthritis development: a comparative study of two strains of guinea piggs with and without spontaneously occuring osteoarthritis. Arthritis Rheum. 2007;56:3366–74.PubMedCrossRefGoogle Scholar
  17. 17.
    Ashraf S, Mapp PI, Walsh DA. Contribution of angiogenesis to inflammation, joint damage, and pain in a rat model of osteoarthritis. Arthritis Rheum. 2011;63:2700–10.PubMedCrossRefGoogle Scholar
  18. 18.
    Walsh DA, McWilliams DF, Turley MJ, et al. Angiogenesis and nerve growth factor at the osteochondral junction in rheumatoid arthritis and osteoarthritis. Rheumatology (Oxford). 2010;49:1852–61.CrossRefGoogle Scholar
  19. 19.
    Zhang R, Fang H, Chen Y, et al. Gene expression analyses of subchondral bone in early experimental osteoarthritis by microarray. PLoS One. 2012;7:e32356.PubMedCrossRefGoogle Scholar
  20. 20.
    Sanchez C, Pesesse L, Gabay O, et al. Regulation of subchondral bone osteoblast metabolism by cyclic compression. Arthritis Rheum. 2012;64:1193–203.PubMedCrossRefGoogle Scholar
  21. 21.
    Baker-LePain JC, Lane NE. Role of bone architecture and anatomy in osteoarthritis. Bone. 2012;51:197–203.PubMedCrossRefGoogle Scholar
  22. 22.
    Patra D, Sandell LJ. Evolving biomarkers in osteoarthritis. J Knee Surg. 2011;24:241–9.PubMedCrossRefGoogle Scholar
  23. 23.
    Sandell LJ. Biomarkers in osteoarthritis. HSS J. 2012;8:33–4.PubMedCrossRefGoogle Scholar
  24. 24.
    Sandell LJ Etiology of osteoarthritis: genetic and synovial joint development. Nat Rev Rheumatol. 2012;8:77–89.PubMedCrossRefGoogle Scholar
  25. 25.
    Daans M, Luyten FP, Lories RJ. GDF5 deficiency in mice is associated with instability-driven joint damage, gait and subchondral bone changes. Ann Rheum Dis. 2011;70:208–13.PubMedCrossRefGoogle Scholar
  26. 26.
    Stecher RM. Heberden’s nodes: hereditary in hypertrophic arthritis of the finger joints. Am J Med Sci. 1941;201:801–9.CrossRefGoogle Scholar
  27. 27.
    Madry H, Luyten FP, Facchini A. Biological aspects of early osteoarthritis. Knee Surg Sports Traumatol Arthrosc. 2012;20:407–22.PubMedCrossRefGoogle Scholar
  28. 28.
    Messier SP, Gutekunst DJ, Davis C, et al. Weight loss reduces knee-joint loads in overweight and obese older adults with knee osteoarthritis. Arthritis Rheum. 2005;52:2026–32.PubMedCrossRefGoogle Scholar
  29. 29.
    Messier SP. Osteoarthritis of the knee and associated factors of age and obesity: effects on gait. Med Sci Sports Exerc. 1994;26:1446–52.PubMedGoogle Scholar
  30. 30.
    Aaboe J, Bliddal H, Messier SP, et al. Effects of an intensive weight loss program on knee joint loading in obese adults with knee osteoarthritis. Osteoarthritis Cartilage. 2011;19:822–8.PubMedCrossRefGoogle Scholar
  31. 31.
    Crema MD, Roemer FW, Felson DT, et al. Factors associated with meniscal extrusion in knee with or at risk for osteoarthritis: the Multicenter Osteoarthritis study. Radiology. 2012:264;494–503.PubMedCrossRefGoogle Scholar
  32. 32.
    Hayashi D, Englund M, Roemer FW, et al. Knee malalignment is associated with an increased risk for incident and enlarged bone marrow lesions in the more loaded compartments: the MOST study. Osteoarthritis Cartilage. 2012;20:1227–33.PubMedCrossRefGoogle Scholar
  33. 33.
    Bijlsma JW, Berenbaum F, Lafeber FP. Osteoarthritis: an update with relevance for clinical practice. Lancet. 2011;377:2115–26.PubMedCrossRefGoogle Scholar
  34. 34.
    Verzijl N, DeGroot J, Ben ZC, et al. Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: a possible mechanism through which age is a risk factor for osteoarthritis. Arthritis Rheum. 2002;46:114–23.PubMedCrossRefGoogle Scholar
  35. 35.
    Zimmermann AE, Schaible E, Bale H, et al. Age-related changes in the plasticity and thoughness of human cortical bone at multiple length scales. Proc Natl Acad Sci U S A. 2011;108:14416–21.PubMedCrossRefGoogle Scholar
  36. 36.
    Kopec JA, Sayre EC, Flanagan WM, et al. Development of a population-based microsimulation model of osteoarthritis in Canada. Osteoarthritis Cartilage. 2010;18: 303–11.PubMedCrossRefGoogle Scholar
  37. 37.
    Nüesch E, Dieppe P, Reichenbach S, et al. All cause and disease specific mortality in patients with knee or hip osteoarthritis: population based cohort study. BMJ. 2011;342:d1165.PubMedCrossRefGoogle Scholar
  38. 38.
    Jaramillo A, Welch VA, Ueffing E, et al. Prevention and self-management interventions are top priorities for osteoarthritis systemic reviews. Journal Clin Epidemiol. 2012. doi: 10.1016/j.jclinepi.2012.06.017Google Scholar
  39. 39.
    Williams NH, Amoakwa E, Belcher J, et al. Activity increase despite arthritis (AЇDA): phase II randomised controlled trial of an active management booklet for hip and knee osteoarthrits in primary care. Br J Gen Pract. 2011;61:e452–8.PubMedCrossRefGoogle Scholar
  40. 40.
    Chyu MC, von Bergen V, Brismée JM, et al. Complementary and alternative exercises for management of osteoarthritis. Arthritis. 2011;2011:364319.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Wien 2012

Authors and Affiliations

  1. 1.Clinical Institute of PathologyMedical University of ViennaViennaAustria

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