Prolotherapy in the treatment of foot problems.

To the Editor: The idea of inducing inflammation of a joint and adjacent structures to allow for the proliferation of scar tissue in an effort to stabilize a joint is not a new one. In the fifth century BC, Hippocrates supposedly treated separated shoulders by cauterizing areas of the shoulder to promote axillary scarring. Sclerotherapy, the injection of areas around the enthesis with an inflammatory agent to promote tensile strength and increase the size of adjacent ligaments, has been used in one form or another since the 1950s in the treatment of arthritic conditions of the back and peripheral joints as well as hernias. Sclerotherapy for hypermobile joints works by strengthening opposing ligament structures. This is similar to strengthening the abdominal muscles when treating low-back problems. Sclerosants are available in various forms and combinations of glucose, glycerine and phenol, morrhuate sodium, polidocanol (hydroxy-polyethoxy-dodecane), and zinc sulfate. An anesthetic is often used in conjunction with the sclerosant to minimize initial discomfort from the injection.1, 2 In order to understand how sclerosants work, it is important to know how the treated joint was weakened. In an arthritic joint, the pain is due to an inflammatory response to the degenerating joint. Corticosteroid injections can decrease the inflammation, but they do not address the degeneration of the joint. If degeneration of the adjacent tissues continues, the joint can lapse into hypermobility, resulting in pain. Hypermobility can be treated with a sclerosing agent used in prolotherapy.1, 2 Histologic studies have shown that an inflammatory response to the sclerosant reaches a peak within 24 hours and subsides at 48 hours. Fibroblast formation that occurs at 3 days precedes the eventual collagen formation at 7 days. Dense fibrous tissues adjacent to the joints are seen at 8 weeks.1 In a study of rabbit ligaments injected with a 5% morrhuate sodium solution and a control group injected with sterile saline solution, Liu et al3 found a substantial difference in mean fibril diameters of injected ligaments (129.9 nm for morrhuate sodium–injected ligaments versus 83.2 nm for controls). Under electron microscopy, collagen fibrils were more densely packed and of a more uniform size in the sclerosed ligaments as compared with the controls. An increase in tensile strength was evident in the sclerosed ligaments as compared with the control ligaments. Therefore, by strengthening adjacent ligaments and decreasing movement at painful joints, painful joint degeneration may be controlled.3