The Composite Hypothesis

The above three hypotheses are not mutually exclusive. An immunologic event may be secondary to cutaneous injury or neural stimulation may lead to overproduction of the toxic precursors in melanocytes with subsequent leakage of an aggressive immunologic process destructive to melanocytes (7SS). 

Alternatively, melanin formation and destruction may be seen as a physiologically precarious balance process with a metastable equilibrium in those genetically disposed towards it. Overstimulation of neural elements, trauma, sunburn etc., may upset this homeostasis in favour of melanin destruction, again with incontinence of antigenic material and resultant immunologic melanocyte destruction (35, 144, 189). 

Finally, it cannot be excluded that the primary event is a deficit in feedback control from keratinocytes to melanocytes, such that whatever mechanism genetically limits the number and packaging of melanosomes 

Although, this composite hypothesis, like the other three hypotheses, lacks experimental support it appears to encompass more of the facts and ahnormalities in vitiliginous patients. 

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