Biomechanical Factors in Psoriatic Disease: Defective Repair Exertion as a Potential Cause. Hypothesis Presentation and Literature Review

Abstract

Joining main clinical manifestations of psoriatic skin disorder are inflammatory arthritis and nail lesions. Repetitive microdamage has been postulated as a main triggering factor in lesions of psoriatic arthritis. This concept of psoriatic disease might also be admissible for triggering nail lesions because the nail is a frequently traumatized structure. Here, we aimed to describe the conjectural injury mechanisms of nail complex with regard to acting biomechanical factors. Tissue repair response to physical microdamage may be altered in psoriatic disease. It is plausible to consider that a defective repair process in the dysregulated prepsoriatic tissue may lead to innate immune activation and further development of autoinflammatory lesions, although excessive inflammation is known to impair wound healing. Recently published data have revealed the importance of mechanosensitive Wingless-type (Wnt) signaling in the pathophysiology of psoriasis and ankylosing spondylitis. The Wnt signaling system is involved in morphogenesis, repair, and regeneration as a biologic process main regulator. Wnt5a seems to be a dominating mediator in both psoriatic plaques and during the spondylitis process that might also be a linking molecule of psoriatic response to mechanical stress. Future studies should focus on complex responsive interactions of tissue repair regulators regarded in psoriatic disease.

Figure 1

A proposed paradigm of altered repair response to chronic mechanical stress through Wnt5a signaling