Table 1.

Chosen aspects of comparative analysis of human perianal Crohn’s disease (pCD) and canine anal furunculosis (AF).

		Humans—Perianal Crohn’s Disease	Ref.	Dogs—Anal Furunculosis	Ref.
Symptoms	Association of perianal disease with bowel inflammation	Established. Only about 5% of patients with perianal CD do not have concurrent luminal form of CD	[1]	Probable. 39% of dogs with diagnosed AF do not present histological symptoms of colitis or endoscopic signs of proctitis	[30]
	Perianal symptoms	Fissures, skin tags, ulcers, abscesses, true fistulas with two openings, anal strictures	[37]	Perianal blind sinuses, ulcerations, fistulas communicating with anal sac or anorectum (the incidence of true fistulas with two openings not established)	[20]
Response to pharmacologic therapy	Antibiotics	Proven to reduce drainage of perianal fistulas, not to induce healing, recommended as adjunctive therapy	[37]	Efficacy not proven, sometimes used as adjunctive therapy	[20]
	Cyclosporine (CsA)	Efficacy not proven—not recommended	[2]	Proven efficacy—recommended	[38]
	Thiopurine derivatives (i.e., azathioprin)	Moderate efficacy—recommended	[39]	Moderate efficacy based on scant data, sometimes used if CsA therapy is not possible (due to economic reasons or availability problems)	[40]
	Anti-TNF	Proven efficacy—recommended	[41]	Not tested, caninized anti-TNF not available
Pathogenesis	Genetic factors	The role of genes encoding MHC molecules (generally for CD)—confirmed	[42]	the role of genes encoding MHC molecules (DLA-DRB1)—confirmed	[43]
		The role of SNPs in NOD2 (one of PPRs) (specifically in pCD) - confirmed	[44]	The role of SNPs in chosen PPRs (including NOD2) failed to be confirmed	[45]
		The role of TNF pathway genes (specifically for pCD)—confirmed	[33]	The role of TNF pathway not confirmed	[46]
		The role of other genes associated with cell adhesion, extracelullar matrix, scaffolding proteins or autophagy indicated (specifically for pCD)	[33]	6 non-synonymous SNPs identified to be related to AF. The most significantly associated genes were ADAMTS16 and CTNND2	[46]
	Intestinal microbiota	Association of gut microbiota with pCD confirmed. Dichotomy of microbiome into dysbiotic and non-dysbiotic reported	[47]	Association of gut microbiota with AF confirmed. Dichotomy of microbiome into dysbiotic and non-dysbiotic reported	[48]
	Disturbances in T cell mediated immunity	Association of abnormal T cell response with pCD confirmed. Excessive Th1 response; Excessive Th17 response	[49]	Association of abnormal T cell response with AF confirmed. Excessive Th1 response; role of Th17 response not studied	[31]
	Metallo-proteinases (MMPs)	Elevated expression of MMP-2, MMP-9, and MMP-13 in pCD fistulas	[50]	Elevated expression of MMP9 and MMP13 but not MMP2 in perianal tissue of dogs with AF	[36]
	Epithelial-to-mesenchymal transition	The EMT process confirmed to be involved in the formation of CD-related fistulas	[51]	The association of EMT process and AF not studied