Neuropeptides like substance P and CGRP, released by sensitised nociceptive C-fibres,24 lead to neuroinflammation with increased cytokine production (TNF-α, interleukin-6) and proliferation or immigration of Langerhans and mast cells.4,15 The presence of IgG antibodies against autonomic nervous system receptors (β2-, α1A-adrenergic, and M2-muscarinic receptors) suggests an autoimmune component in some patients with CRPS.10,20 These mechanisms may collectively contribute to varying degrees of bone loss, independent of injury location and CRPS type. This evidence concerns the gene CHRM2 and complex regional pain syndrome.