A four-year-old male cat (Felis vulgarism).A four-year-old male cat was presented with thickening and erythema of the inner surfaces of the left ear.
The ear was painful and curled. The outer surfaces were unaffected. The left pinna was partially removed and
submitted for histopathology.
Besides the thickened and curled left ear with erythema, there were no other grossly visible
The lesion is centered around the pinnal cartilage.Â It consists of an
inflammatory infiltration of mainly neutrophils and moderate numbers of macrophages, multinucleated giant cells
(foreign body type), lymphocytes and plasma cells.Â Several neutrophils are invading the pinnal cartilage.Â The latter
is irregularly lined, angularly deformed (wrinkled and curled over 180 degrees) and possesses a loss of basophilia
(cartilage degeneration).Â Collagenous tissue surrounds the pinnal cartilage (perichondrial fibrosis).Â The dermis is
edematous and diffusely infiltrated by neutrophils, lymphocytes and plasma cells.Â Perivascular accumulations of
mononuclear and polymorphonuclear cells are present.
Pinna: diffuse, chronic, suppurative to granulomatous chondritis with
degeneration and deformation of the pinnal cartilage.
Feline relapsing polychondritis
Feline relapsing polychondritis is a very rare disease and only a few reports of cats with
the disease are found in the literature(2, 3).Â There is no sex predilection for the disease, but predominantly young to
middle aged cats are affected(3).Â In humans, the disease is believed to be an immune-mediated disease of type II
collagen, which is restricted to cartilage(2, 3).
Sometimes the disease is also called auricular chondritis, because the main gross lesions are ear swelling and discoloration, erythema, pain and curling of one or both ears.Â However, two case reports describe involvement of additional cartilaginous tissues as reported in people(1, 3).
Histologically, there is degeneration, loss of basophilic staining and necrosis of the ear cartilage.Â There is also infiltration of mononuclear and polymorphonuclear cells, and perichondrial and perivascular fibrocyte and capillary endothelial cell proliferation.Â The histological lesions observed in this case are similar to those reported in the cases described in the literature.
Ear, pinna: Cellulitis, chronic-active, diffuse, moderate with mild neutrophilic chondritis, cartilage
degeneration, and granulation tissue.
Conference participants discussed the comparative pathology of feline relapsing
polychondritis and auricular chondritis of laboratory rodents, to which some strains of mice, and aged Sprague-
Dawley, Wistar, and fawn-hooded rats are predisposed(4).
In rats, trauma from cagemates or metal ear tags is suspected as the inciting cause of auricular chondritis, but the disease frequently occurs without history or evidence of trauma.Â Unlike the feline disease, auricular chondritis in rats is always bilateral, even when the metal ear tag is present in only one ear, and increases in incidence with age(5). The disease presents grossly as firm, multinodular to diffuse thickening of pinnae, and bilateral lesions extend peripherally from the base of the pinnae.Â Occasionally, pinnae are uniformly thickened rather than having nodular lesions.Â There is degeneration and lysis of the auricular cartilage plate with granulomatous inflammation and proliferative immature cartilaginous nodules and fibrosis, and osseous metaplasia is characteristic in advanced lesions(5).
Auricular chondritis in rats has been proposed as a model for relapsing polychondritis in humans, which involves several cartilage-containing tissues, including the ear(5).Â In humans, relapsing polychondritis is associated with auricular chondritis, inflamed cartilage in other sites, and antibodies to type II collagen, IgG and C3 complement. Antibodies to type II collagen have not been demonstrated in the spontaneous auricular chondropathy of rats, and unlike relapsing polychondritis in humans, only the auricular cartilage is involved(4, 5).
In mice, it is speculated that metal ions from ear tags, such as copper and iron, incite an autoimmune process via activation of matrix metalloproteinases.Â These metal ions supply reactive oxygen species that induce inflammation and fibrosis, and oxidation of cartilage collagen renders the collagen fibrils more brittle and prone to mechanical fatigue.Â Tagged ears have increased amounts of metallothionein (MT-I and MT-II) and increased expression of Th1 cytokines, including interferon-Î³, tumor necrosis factor-Î±, and interleukin-2; it is postulated that the lesion represents a delayed-type allergic contact dermatitis in response to the metal ions(4).Â There are two proposed mechanisms for the fibrosis and osseous metaplasia seen in advanced lesions.Â In the first, cartilage degeneration, characterized by chondrolysis and splitting of the pinnal cartilage plate leads to perichondrial fibrous proliferation, which differentiates into fibroadipose tissue and progresses to fibrochondrous and/or osseochondrous tissue.Â In the second proposed mechanism, there is focal granulomatous inflammation without chondrolysis, and fibroblasts proliferate within the granulomatous inflammation and then differentiate into fibrochondrous tissue with subsequent chondrous and osseous differentiation(5).
1.Â Baba T, Shimizu, A, Ohmuro T, Uchida N, Shibata K, Nagata M, Shirota K: Auricular chondritis associated with systemic joint and cartilage inflammation in a cat J.Â Vet.Â Med.Â Sci. 1:79-82, 2009.
2.Â Delmage DA and Kelly DF: Auricular chondritis in a cat.Â Journal of Small Animal Practice 42:499-501, 2001.
3.Â Gerber B, Crottaz M, von Tscharner C, Sch+ï¿½-ï¿½rer V: Feline relapsing polychondritis: two cases and a review of literature.Â Journal of Feline Medicine and Surgery 4:189-194, 2002.
4.Â Kitagaki M, Hirota M.Â Auricular chondritis caused by metal ear tagging in C57BL/6 mice.Â Vet Pathol. 2007; 44:458-466.
5.Â Kitagaki M, Suwa T, Yanagi M, Shiratori K.Â Auricular chondritis in young ear-tagged Crj:CD (SD)IGS rats.Â Lab Anim Sci.Â 2003; 37(3): 249-253.