Osteoarthropathy

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Luke Clancy - One of the best experts on this subject based on the ideXlab platform.

Paul T Kelly - One of the best experts on this subject based on the ideXlab platform.

Michael Edmonds - One of the best experts on this subject based on the ideXlab platform.

  • inflammatory and bone turnover markers in a cross sectional and prospective study of acute charcot Osteoarthropathy
    Diabetic Medicine, 2015
    Co-Authors: Nina L. Petrova, Tracy Dew, Roy Sherwood, Rebecca Musto, Maureen Bates, C. Moniz, Michael Edmonds
    Abstract:

    Aims To assess markers of inflammation and bone turnover at presentation and at resolution of Charcot Osteoarthropathy. Methods We measured serum inflammatory and bone turnover markers in a cross-sectional study of 35 people with Charcot Osteoarthropathy, together with 34 people with diabetes and 12 people without diabetes. In addition, a prospective study of the subjects with Charcot Osteoarthropathy was conducted until clinical resolution. Results At presentation, C-reactive protein (P = 0.007), tumour necrosis factor-α (P = 0.010) and interleukin-6 (P = 0.002), but not interleukin-1β, (P = 0.254) were significantly higher in people with Charcot Osteoarthropathy than in people with and without diabetes. Serum C-terminal telopeptide (P = 0.004), bone alkaline phosphatase (P = 0.006) and osteoprotegerin (P < 0.001), but not tartrate-resistant acid phosphatase (P = 0.126) and soluble receptor activator of nuclear factor-κβ ligand (P = 0.915), were significantly higher in people with Charcot Osteoarthropathy than in people with and without diabetes. At follow-up it was found that tumour necrosis factor-α (P = 0.012) and interleukin-6 (P = 0.003), but not C-reactive protein (P = 0.101), interleukin-1β (P = 0.457), C-terminal telopeptide (P = 0.743), bone alkaline phosphatase (P = 0.193), tartrate-resistant acid phosphatase (P = 0.856), osteoprotegerin (P = 0.372) or soluble receptor activator of nuclear factor-kβ ligand (P = 0.889), had significantly decreased between presentation and the 3 months of casting therapy time point, and all analytes remained unchanged from 3 months of casting therapy until resolution. In people with Charcot Osteoarthropathy, there was a positive correlation between interleukin-6 and C-terminal telopeptide (P = 0.028) and tumour necrosis factor-α and C-terminal telopeptide (P = 0.013) only at presentation. Conclusions At the onset of acute Charcot foot, serum concentrations of tumour necrosis factor-α and interleukin-6 were elevated; however, there was a significant reduction in these markers at resolution and these markers may be useful in the assessment of disease activity.

  • Inflammatory and bone turnover markers in a cross-sectional and prospective study of acute Charcot Osteoarthropathy.
    Diabetic medicine : a journal of the British Diabetic Association, 2014
    Co-Authors: Nina L. Petrova, Tracy Dew, Roy Sherwood, Rebecca Musto, Maureen Bates, C. Moniz, Michael Edmonds
    Abstract:

    Aims To assess markers of inflammation and bone turnover at presentation and at resolution of Charcot Osteoarthropathy. Methods We measured serum inflammatory and bone turnover markers in a cross-sectional study of 35 people with Charcot Osteoarthropathy, together with 34 people with diabetes and 12 people without diabetes. In addition, a prospective study of the subjects with Charcot Osteoarthropathy was conducted until clinical resolution. Results At presentation, C-reactive protein (P = 0.007), tumour necrosis factor-α (P = 0.010) and interleukin-6 (P = 0.002), but not interleukin-1β, (P = 0.254) were significantly higher in people with Charcot Osteoarthropathy than in people with and without diabetes. Serum C-terminal telopeptide (P = 0.004), bone alkaline phosphatase (P = 0.006) and osteoprotegerin (P 

  • CHARCOT Osteoarthropathy: ONE DISEASE, TWO PRESENTATIONS
    Biomedical Reviews, 2005
    Co-Authors: Nina L. Petrova, Michael Edmonds
    Abstract:

    Charcot Osteoarthropathy or Charcot foot is a disabling complication of diabetes and is associated with poor prognosis and high mortality. Its pathogenesis is not fully understood and its treatment is at best symptomatic. Furthermore, it is not known whether there is a specific type of neuropathy which affects osteoclastic activity, and thereby leads to reduction of bone mineral density and the development of Charcot Osteoarthropathy. Recently it has been proposed that there is a difference in the presentation of Charcot Osteoarthropathy between type 1 and type 2 diabetes. This article reviews the link between underlying osteopenia, abnormal biomechanical forces and type of neuropathy, and their varying interaction in the pathogenesis of Charcot Osteoarthropathy in type 1 and type 2 diabetes. Further attention is drawn to the newly discovered osteoprotegerin/receptor activator of nuclear factor kappaB ligand (OPG/RANKL) cytokine system, which controls bone resorption. Increased osteoclastic activity in the acute Charcot foot may be associated with altered expression of OPG/RANKL signaling pathway and modulation of the OPG/RANKL equilibrium in Charcot Osteoarthropathy may provide additional therapeutical option to manage this difficult condition. Biomedical Reviews 2005; 16: 43-48.

Patricia Corcoran - One of the best experts on this subject based on the ideXlab platform.

Patrick J Manning - One of the best experts on this subject based on the ideXlab platform.