PEH was described originally as a skin disease with an exuberant proliferation of epidermal tissue(29) and has been reported as a rare complication of fistulated chronic osteomyelitis distinct from neoplastic lesions in the jawbone.(30) Akilov and colleagues (2007) demonstrated in the experimental cutaneous leishmaniasis mouse model that intralesional injections of TNF-α and IFN-γ initiated PEH in mouse ear skin.(31) The upregulation of TNF-α and IFN-γ in postextraction oral mucosa of the VitD(−)/ZOL group (Fig. 4) appears to provide a pathologic mechanism to develop PEH in our model. Here, TNF is linked to cutaneous leishmaniasis.