Enni Sanmark1, Johanna Wikstèn1, Hannamari Välimaa2,3, Karin Blomgren1. 1. a Department of Otorhinolaryngology - Head and Neck Surgery, Helsinki University Hospital , Helsinki , Finland. 2. b Department of Virology, University of Helsinki , Helsinki , Finland. 3. c Department of Oral and Maxillofacial Surgery, University of Helsinki and Helsinki University Hospital , Helsinki , Finland.
Abstract
Aim: The purpose of this prospective study was to determine if there is a difference in number and distribution of salivary bacteria between patients with tonsillar infection and healthy volunteers. Background: The etiology of peritonsillar abscess (PTA) is unclear. Smoking, periodontal disease, and infection of minor salivary glands have been suggested as predisposing factors for PTA. Material and methods: Patients with acute tonsillitis (AT) (n = 54), peritonsillitis (PT) (n = 36), PTA (n = 58), and healthy volunteers (n = 52) were prospectively recruited and evaluated. Saliva bacteria were analyzed with flow cytometry. Patients and their treating physicians completed a questionnaire about patients' current disease, smoking habits, alcohol consumption, and oral health. Results: There were no differences in the total number of saliva bacteria between patients with acute throat infection and healthy volunteers (p = .104) or between AT, PT, and PTA patients (p = .273). Smoking habits, alcohol consumption, oral hygiene, or prior antibiotics had no effect on total amount of salivary bacteria in patients with acute throat infection. Conclusions: The effects of smoking on salivary bacteria do not seem to be the mechanism that promotes development of PTA in smokers.
Aim: The purpose of this prospective study was to determine if there is a difference in number and distribution of salivary bacteria between patients with tonsillar infection and healthy volunteers. Background: The etiology of peritonsillar abscess (PTA) is unclear. Smoking, periodontal disease, and infection of minor salivary glands have been suggested as predisposing factors for PTA. Material and methods: Patients with acute tonsillitis (AT) (n = 54), peritonsillitis (PT) (n = 36), PTA (n = 58), and healthy volunteers (n = 52) were prospectively recruited and evaluated. Saliva bacteria were analyzed with flow cytometry. Patients and their treating physicians completed a questionnaire about patients' current disease, smoking habits, alcohol consumption, and oral health. Results: There were no differences in the total number of saliva bacteria between patients with acute throat infection and healthy volunteers (p = .104) or between AT, PT, and PTA patients (p = .273). Smoking habits, alcohol consumption, oral hygiene, or prior antibiotics had no effect on total amount of salivary bacteria in patients with acute throat infection. Conclusions: The effects of smoking on salivary bacteria do not seem to be the mechanism that promotes development of PTA in smokers.