Immunohistochemical evaluation of mononuclear infiltrates in canine lupoid onychodystrophy

The purpose of this study was to characterize the immunophenotype of the inflammatory infiltrate in canine lupoid onychodystrophy and to determine if decalcification interferes with immunoreactivity. Claw biopsies of 14 dogs with lupoid onychodystrophy were stained with CD3, BLA36 and HM57 (CD97α), MAC 387, lysozyme and MHC class II using an immunoperoxidase and avidin/biotin technique. Cells infiltrating the claw matrix were counted in two high‐power fields; numbers were expressed as a percentage of the cellular infiltrate. The inflammatory infiltrate consisted predominantly of B and T cells; macrophages were typically only present in small numbers. There was no correlation between the predominant inflammatory cell and clinical parameters. CD3, BLA36, lysozyme and MHC II preserved significant antigenicity during formalin fixation and short decalcification, while staining for CD79A and particularly MAC 387 was less reliable. Prolonged decalcification of 7–14 days abolished immunostaining with all antibodies. Short decalcification periods allow immunostaining of samples with some antibodies (CD3, BLA36, lysozyme, MHC II), but not others (CD79A, MAC387), while prolonged decalcification prohibits immunostaining. The nature of the mononuclear infiltrate in lupoid onychodystrophy is not helpful clinically. This study was funded by the American Academy of Veterinary Dermatology.