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Neurovascular invasion at the osteochondral junction and in osteophytes in osteoarthritis
  1. Sunita Suri1,*,
  2. Sarah E Gill1,*,
  3. Sally Massena de Camin1,
  4. Daniel F McWilliams1,
  5. Deborah Wilson2,
  6. David A Walsh1,2
  1. 1
    Academic Rheumatology, University of Nottingham, City Hospital, Hucknall Road, Nottingham, Notts NG5 1PB, UK
  2. 2
    Back Pain Unit, King’s Mill Hospital, Sutton in Ashfield, Notts NG17 4JL, UK
  1. Dr D A Walsh, Academic Rheumatology, University of Nottingham Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham, Notts NG5 1PB, UK; David.Walsh{at}


Background: Normal adult articular cartilage is thought to be avascular and aneural.

Objective: To describe neurovascular structures at the osteochondral junction and in osteophytes in tibiofemoral osteoarthritis (OA) displaying a range of severity of cartilage changes.

Methods: Articular surfaces were obtained from 40 patients at total knee joint replacement surgery for tibiofemoral OA (TKR) and seven patients post mortem (PM). Antibodies directed against CD34 (vascular endothelium), protein gene product 9.5 (pan-neuronal marker), substance P and calcitonin gene-related peptide (sensory nerves) and C-flanking peptide of neuropeptide Y (sympathetic nerves) were used to localise blood vessels and nerves by immunohistochemistry. Severity of OA cartilage changes was graded histologically.

Results: TKR and PM samples displayed a range of OA cartilage changes including tidemark breaching by vascular channels. Sympathetic and sensory nerves were both present within vascular channels in the articular cartilage, in both mild and severe OA. Perivascular and free nerve fibres, and nerve trunks were observed within the subchondral bone marrow and within the marrow cavities of osteophytes. Sensory and sympathetic nerves displayed similar distributions in each region studied.

Conclusion: Vascularisation and the associated innervation of articular cartilage may contribute to tibiofemoral pain in OA across a wide range of structural disease severity.

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  • Competing interests: None.

  • *These two authors contributed equally to this work.

  • Abbreviations:
    total knee joint replacement
    C-flanking peptide of neuropeptide Y
    calcitonin gene-related peptide
    PGP 9.5
    pan-neuronal marker protein gene product 9.5
    phosphate-buffered saline
    streptavidin–biotin complex