Response to Dr Sundberg's Letter to the Editor:.

This response is intended to clarify your questions regarding our recent paper. The association we demonstrated between hair-induced oronasal lesions and ulcerative dermatitis (UD) in C57BL/6 mice was based on a scoring system we developed to better assess the hair-induced lesions. This scale was constructed using criteria that characterized the severity of the lesions based on the inflammatory and tissue responses against the foreign body.1 We understand that gingival hair impaction could be a “universal” background lesion in the majority, if not all, mouse strains, as a consequence of their grooming activity towards themselves and others.5 However, when these lesions progress to a chronic condition, many other destructive processes develop, including severe inflammation, bone destruction and remodeling, and oralnasal fistulas. These processes may have a marked impact on the overall health status of the animals, including immune effects, pain, and a drive to eliminate the irritation by scratching. C57Bl/6 mice are known not only as excessive groomers3 and potential models for trichotillomania,2 but also for their prominent Th1 immune response,8 which could result in the expression of a completely different cytokine array compared to other strains with the same type of insult. Our observations led us to conclude that mice with UD had higher scores in relation to inflammation and their hair-induced oronasal lesions, and on that basis we established the association.1 The clinical and pathologic characterization of B6 alopecia and dermatitis that you describe6,7 differs greatly from our characterization of UD. Animals we have observed usually develop lesions as adults, and the lesions are not a progressive alopecia that leads to ulceration, but instead present as severe pruritus with a rapid onset of skin excoriation that progresses to ulceration overnight or within a 2- to 3-d period.4 Lesions can occur on different parts of the body but are mainly between the shoulders. The response to antiinflammatory treatment(s) varies by location, and dorsocervical lesions tend to repair better than lesions located in other areas.4 Trimming the toenails to prevent self trauma has resulted in lesion improvement, further suggesting that we are discussing a different lesion than the one you describe. Histologically we do not see folliculitis/furunculosis, chronic dermal fibrosis or inflammation directed at the adnexa. Also, the incidence we see is lower than would be expected if the cause was a genetic deficiency of an enzyme, which would be universally present along the population of mice and uniformly distributed in the skin. Although we evaluated some of the references you cited when writing our paper, we felt that the lesions described in those citations were completely different both grossly and histologically from those we see in our facility. The association we established between oralnasal lesions and UD opens a window for us to study the possibility of an exacerbated systemic inflammatory response, triggered by a local insult as the cause of UD in C57BL/6 mice. We are working on this hypothesis and hope to have conclusive results soon. Letters to the Editor Letters discuss material published in CM in the previous 3 issues. They can be submitted through email (gro.salaa@slanruoj) or by regular mail (9190 Crestwyn Hills Dr, Memphis, TN 38125). Letters are not necessarily acknowledged upon receipt nor are the authors necessarily consulted before publication. Whether published in full or part, letters are subject to editing for clarity and space. The authors of the cited article will generally be given an opportunity to respond in the same issue in which the letter is published. Sincerely, Sandra Duarte-Vogel, DVM Clinical Veterinarian, Division of Laboratory Animal Medicine, David Geffen School of Medicine at UCLA Gregory W Lawson DVM, PhD, DACLAM Executive Associate Director, Division of Laboratory Animal Medicine David Geffen School of Medicine at UCLA