Keloids

Volume: 2
Issue: 5
May 15, 2007
Keloids

Dear Colleagues:

 

It is always interesting to see a new scientific explanation come forward to explain an old clinical observation. Although western medicine prides itself on its scientific underpinnings, it is not unusual for science to follow clinical practice rather than to lead it. 

A case in point is neural therapy of keloids. The early neural therapists noticed that the scars they were injecting, (with the aim of treating interference fields), serendipitously softened and shrank the connective tissue.  his observation lead to injection of keloid scars for cosmetic reasons alone.

Dupuytren’s contractures resemble keloids in that both exhibit excessive growth of connective tissue and both respond to injections of procaine. Dosch in his textbook “Manual of neural therapy”, considered the abnormal connective tissue proliferation to be due to “chronic inflammation”. Procaine has been known to possess anti-inflammatory properties since 1906, but the cellular pathophysiology underlying Dupuytren’s and keloids has only been elucidated in recent decades.

The etiology of Dupuytren’s disease is somewhat of a mystery. There is a strong hereditary component.  Most victims are of Celtic or Scandinavian origin and the male to female ratio is 5:1. Occasionally Dupuytren’s seems to be triggered by trauma, especially vibratory trauma, but most of the time onset is spontaneous.  And although Dupuytren’s shares with keloids the characteristic of excessive collagen deposition, it differs in that the connective tissue contracts.

A key player in “fibrocontractive diseases” such as Dupuytren’s and Peyronie’s disease is the myofibroblast, a cell differentiated from fibroblasts by mechanical stress, the action of a cytokine, TGF-β, (which is also involved in triggering collagen formation) and by cellular fibronectin. The myofibroblast plays a physiological role in the remodeling of connective tissue; e.g. in granulation tissue it contracts, thereby shrinking the size of the wound as it heals. The molecule responsible for contraction is alpha smooth muscle actin, a form of actin normally found in smooth muscle.

Myofibroblasts are under sympathetic nervous system control and contract in the presence of adrenaline and angiotensin.  When wound healing is complete, these cells normally disappear through apoptosis. It has been suggested that in fibrocontractive diseases, that this mechanism fails, leading to persisting myofibroblasts. Therefore just as beta blockers may impair wound healing, abnormal sympathetic signals may create an “excessive healing” response by promoting abnormal myofibroblastic activity.

Neural therapy has also been called “regulation therapy” and for good reason. Abnormal autonomic nervous system activity, (whether hyper- or hypo-) can be regulated by injecting procaine into the site of tissue disturbance. In the case of Dupuytren’s contracture, repeat injections directly into the nodule in the palmar fascia and at intervals along the course of the flexor tendons will result in reduction in the contracture and softening of the tissues. It is not necessary to infiltrate all of the affected tissue. Dosch has suggested adding hyaluronidase to the procaine. Of course, the earlier the intervention in the progression of the illness, the better the response.
 

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