A pilot study including conventionally reared, germ free and SCID mice demonstrated that commensal microbial colonization influences https://www.selleckchem.com/products/psi-7977-gs-7977.html the click here expression of innate host defense mediators at both the mRNA and the protein level in the periodontal tissues [17]. In a non-oral setting, a number of studies have examined the transcriptional profiles in response to

microbial stimuli in intestinal [18–22], gastric [23] and corneal epithelia [24]. In this publication, we expand our earlier work and investigate the association between the subgingival bacterial profile of the periodontal pocket and the whole genome transcriptome of the gingival tissue that is in intimate contact with the microbial biofilm. Methods The study design was approved by the Institutional Review Board of the Columbia University Medical Center. Subjects 120 subjects with moderate to severe periodontitis [65 (54.2%) with chronic

and 55 with aggressive periodontitis] were recruited among those referred to the Post-doctoral Periodontics Clinic of the Columbia University College of Dental Medicine. Eligible patients were (i) >13 yrs old; (ii) had ≥24 teeth; (iii) had no history of systematic periodontal therapy other than occasional prophylaxis, (iv) had received no systemic antibiotics or anti-inflammatory drugs for ≥6 months, (v) harbored GDC 0032 ≥4 teeth with radiographic bone loss, (vi) did not have diabetes or any systemic condition that entails a diagnosis of “”Periodontitis as a manifestation of systemic diseases”" [25], (vii) were not pregnant, and (ix) were not current users of tobacco products or nicotine replacement medication. Signed informed consent Bumetanide was obtained prior to enrollment. Clinical

examination All participants underwent a full-mouth examination of the periodontal tissues at six sites per tooth by a single, calibrated examiner. Variables recorded included presence/absence of visible dental plaque (PL), presence/absence of bleeding on probing (BoP), probing depth (PD), and attachment level (AL). Data were entered chair-side to a computer and stored at a central server. Gingival tissue donor areas and tissue sample collection Subsequently to clinical data entry, a specially developed software identified periodontally ‘diseased’ and ‘healthy’ tooth sites based on the clinical data. ‘Diseased’ sites showed BoP, had interproximal PD ≥4 mm, and concomitant AL ≥3 mm. ‘Healthy’ sites showed no BoP, had PD ≤4 mm and AL ≤2 mm. Next, the software identified (i) maxillary ‘diseased’ and ‘healthy’ interdental papillae, based on the above criteria, and (ii) pairs of diseased interdental papillae with similar clinical presentation (PD and AL within 2 mm of each other). A posterior maxillary sextant encompassing a pair of qualifying ‘diseased’ interdental papillae was identified.