Feline chronic gingivostomatitis: a thorough systematic review of associated factors

Objectives The aim of the present study was to systematically compile and analyze the available evidence from studies that have explored factors associated with feline chronic gingivostomatitis (FCGS). Methods An electronic search was conducted using four databases (OVID/MEDLINE, PubMed, SciELO, Redalyc), as well as proceedings from the European Veterinary Dentistry Forum and the Veterinary Dental Forum, when available. The inclusion and exclusion criteria were predetermined and maintained throughout the systematic process, focusing exclusively on articles published in peer-reviewed journals. Results A total of 17 articles met the definitive inclusion criteria. All were published in English, in 11 journals, and between 1984 and 2023. The relevant articles reported a global frequency of FCGS of 10.9% (747/6881 cats). Six studies reported the exploration of factors inherent to the cat (eg, age, sex, reproductive status), two reported the exploration of factors related to the cats’ environment, feeding and management (eg, type of confinement, number of cats in the household, vaccination status) and 15 reported the exploration of factors related to infectious agents (eg, feline calicivirus [FCV], feline leukemia virus [FeLV], feline herpesvirus type 1 [FHV-1], Bartonella species, Pasteurella multocida subspecies multocida ) and microbiome profiling. Conclusions and relevance Although the specific etiology of FCGS remains unknown, factors involved in the disease suggest that oral microbiome dysbiosis and the presence of infectious agents such as Fusobacterium nucleatum , Porphyromonas species and P multocida , as well as FCV and FHV-1, play crucial roles in its pathogenesis. In addition, factors involving the cat’s immune status, including coinfection with feline immunodeficiency virus and FeLV, have been associated with an increased risk of developing FCGS. Microbial dysbiosis and the alteration of local and systemic immune responses emerge as key elements that perpetuate chronic inflammation. Furthermore, the relationship with non-infectious factors must be considered to understand the complex origin of the disease.