Editing Leprosy (section)

== Mechanism ==
Most leprosy complications are the result of nerve damage. The nerve damage occurs from direct invasion by the ''M. leprae'' bacteria and a person's immune response resulting in inflammation.<ref name="Rei2019"/> The molecular mechanism underlying how ''M. leprae'' produces the symptoms of leprosy is not clear,<ref name=Rod2011/> but ''M. leprae'' has been shown to bind to [[Schwann cell]]s, which may lead to nerve injury including [[demyelination]] and a loss of nerve function (specifically a loss of [[axon]]al conductance).<ref name="pmid22988457">{{cite journal | vauthors = Bhat RM, Prakash C | title = Leprosy: an overview of pathophysiology | journal = Interdisciplinary Perspectives on Infectious Diseases | volume = 2012 | pages = 181089 | date = 2012 | pmid = 22988457 | pmc = 3440852 | doi = 10.1155/2012/181089 | doi-access = free }}</ref> Numerous molecular mechanisms have been associated with this nerve damage including the presence of a [[laminin]]-binding protein and the glycoconjugate (PGL-1) on the surface of ''M. leprae'' that can bind to laminin on [[peripheral nerves]].<ref name="pmid22988457"/>

As part of the human immune response, [[white blood cell]]-derived [[macrophage]]s may engulf ''M. leprae'' by [[phagocytosis]].<ref name="pmid22988457"/> In the initial stages, small sensory and [[autonomic nerve]] fibers in the skin of a person with leprosy are damaged.<ref name="Rei2019" /> This damage usually results in hair loss to the area, a loss of the ability to sweat, and numbness (decreased ability to detect sensations such as temperature and touch). Further peripheral nerve damage may result in skin dryness, more numbness, and muscle weaknesses or paralysis in the area affected.<ref name="Rei2019" /> The skin can crack and if the skin injuries are not carefully cared for, there is a risk for a secondary infection that can lead to more severe damage.<ref name="Rei2019" />