VN November 2022

Vetnews | November 2022 35 on matrix metalloproteinases 2 and 9, Veterinary Ophthalmology (2015) 18, 3, 229–233] 3] Distichiae in dogs – some interesting facts to consider The presence of extra cilia erupting from the tarsal margin of dogs does not always cause pathology. Still, it may result in chronic irritation, lacrimation, and serious damage to the cornea, causing corneal erosions and ulcerations with keratitis. Have you ever thought how they erupt from that location? In serial sample sections for histological examination of cilia- bearing tarsoconjunctival tissue, it was shown that anatomic segments of hair follicles were located abnormally in the eyelid tarsus and associated with the aberrant cilia. They appeared as hair bulbs adjacent to tarsal glands, middle portions of hair follicles located between sebaceous lobules, and single or multiple hair shafts present within the sebaceous duct. They were present in the vicinity of the tarsal glands to which they were connected by their middle segment that finally merged with the excretory duct of these glands. This allowed the aberrant cilia to pass within the excretory duct of the tarsal glands, which correlates with the clinical observations that the distichiatic lashes most often emerge from the openings of the tarsal glands on the lid margin. In addition, they showed that the tarsal glands in the cilia- bearing tarsoconjunctiva were not different from those of the controls, in which no distichiatic hair bulbs or shafts were observed. It confirms that the cilia do not affect the tarsal glands and function. These results demonstrate that adventitious cilia are not associated with histologic changes of the tarsal glands and appear to arise from ectopic hair follicles in the tarsus. But what causes this to occur? Canine distichiasis may result from anomalous regulation of morphogenesis of hair follicles in the mesenchymal tissue of the tarsal plate.During eyelid embryogenesis, the tarsal plate arises from the mesenchymal tissue of the neural crests, while the tarsal glands (i.e. the sebaceous glands) develop by the proliferation of the surface ectoderm from the lid margin into the tarsal plate. It has been shown that cellular differentiation is controlled by a balance of multipotent progenitor [promoting] and repressors of the hair placode formation, which is the first morphological sign of hair follicle development. Thus, if we assume that the molecular mechanisms regulating hair follicle morphogenesis in the skin may also occur in the eyelid, absence of hair follicle development in the healthy tarsal plate could theoretically result from the activation of hair placode repressor(s). Conversely, the formation of ectopic hair follicles in the distichiatic tarsal plate could result from the ectopic expression of factor(s) activating placode promoters or inhibiting placode repressors.It may be controlled by gene expression in the follicular epithelium. Because distichiae can be seen at all ages, this suggests that the mechanism(s) of their morphogenesis within the tarsal plate could continue into adult life. This agrees with data showing that the hair follicle can be generated throughout adult life by differentiation of the progenitor cells in the skin. It may certainly explain why some animals that have had cilia removed by electroepilation or cryotherapy may show further growth and erupting of cilia. It has been postulated that distichiae may have a hereditary component being autosomal dominant with incomplete penetrance.It has been suspected in several breeds, namely Pekingese, English Bulldog, Rough Collie, Shetland Sheepdog, Miniature Longhaired Dachshund, both the English and American Cocker Spaniels and Tibetan Terriers. [Ref: Histopathologic features of canine distichiasis Veterinary Ophthalmology (2012) 15, 2, 92–97] v Regulars I Ophthalmology Column