Abstract
Actinic damage (actinic elastosis) affecting the internal elastic lamina appears to be the prime cause of age change and arteritis of the temporal artery. Resorption and removal of altered elastin (elastolysis) is an integral part of the pathology of actinic damage. Actinic irradiation is probably responsible for the destruction and disappearance of a vast number of arterioles in elastotic skin. The intimate connection between temporal arteritis and polymyalgia rheumatica prompts the belief that the vascular and other internal malign components of the temporal arteritis/polymyalgia rheumatica syndrome might likewise be due, albeit indirectly, to the same actinic cause. Actinic elastotic damage at the body surface could have this effect by provoking a state of systemic elastolysis. Although UV light is often regarded as the sole cause of actinic elastosis, penetrating IR (heat) irradiation may deserve a large or even a dominant share of the blame.

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