Chronic tonsillitis, etiological and pathogenetic aspects of the development of metatonsillar complications

Abstract

The objective of the present study was to summarize the data of the current literature publications concerning the tonsillar biotope under the normal conditions and in the course of the development of the pathological process. Specific microbiological characteristics of the potential causative agents of tonsillar pathology are considered. The structural, immunological, and genetic prerequisites for the for progress of infection are discussed with special reference to the morphological and functional changes in the tissue of palatine tonsils associated with different forms of the disease and the mechanisms underlying immunopathological conditions and metatonsillar complications.

At Early Rheumatoid Arthritis Stage, the Infectious Spectrum Is Driven by Non-Familial Factors and Anti-CCP Immunization

“…Chronic tonsillitis exacerbations. First, in chronic tonsillitis provocation, non-infectious factors play a significant role, in particular, smoking and the intake of damaging volatile pollutants (of a domestic and professional nature) [64,65]. The same factors act as RA triggers.…”

“…Second, recurrent acute bacterial and viral infections are also important. In chronic tonsillitis, these are adenoviruses, influenza, and parainfluenza viruses, Epstein-Barr viruses, herpes simplex viruses, and enteroviruses of I, II, and V serotype, paving the way for S. aureus è S. pyogenes, Fusobacterium necrophorum, Prevotella intermedia, Prevotella histicola, as well as Mycoplasma pneumoniae, and Chlamydia pneumonia [65].…”

“…Chronic inflammation leads to sclerosis of the parenchyma and a disruption of the cytoarchitectonics of the tonsils, interfering with the normal interplay of the lymphoid and non-lymphoid cells involved in the production of necessary cytokines (the signs of immunodeficiency of the tonsil parenchyma), together with the formation of autoimmune humoral and cellular reactions against the tonsil tissue, and the proliferation of connective tissue antigens. In the local immune organs, the signs of Th2 activity, namely plasmocyte activation, were demonstrated [65].…”