Microbiome at sites of gingival recession in children with Hutchinson–Gilford progeria syndrome. Issue 6 (10th July 2018)

• Record Type: Journal Article
• Authors: Bassir, Seyed Hossein; Chase, Isabelle; Paster, Bruce J.; Gordon, Leslie B.; Kleinman, Monica E.; Kieran, Mark W.; Kim, David M.; Sonis, Andrew
• Is Part Of: Journal of periodontology. Volume 89:Issue 6(2018)
• Page Start: 635
• Page End: 644
• Publication Date: 2018-07-10
• Subjects: gingival recession -- Hutchinson–Gilford progeria syndrome -- microbiota -- periodontal diseases -- progeria; Periodontics -- Periodicals; 617.632
• DOI: 10.1002/JPER.17-0351
• Languages: English
• ISSNs: 0022-3492

Abstract

Abstract: Background: Hutchinson–Gilford progeria syndrome (HGPS) is a rare premature aging disorder with significant oral and dental abnormalities. Clinical symptoms include various features of accelerated aging such as alopecia, loss of subcutaneous fat, bone abnormalities, and premature cardiovascular disease. In addition, children with HGPS have been observed to suffer from generalized gingival recession. Whether periodontal manifestations associated with this syndrome are the results of changes in the oral flora is unknown. The present study aimed to identify the microbial composition of subgingival sites with gingival recession in children with HGPS. Methods: Nine children with HGPS were enrolled in this study. Plaque samples were collected from teeth with gingival recession. DNA samples were analyzed using the Human Oral Microbe Identification Microarray (HOMIM). Microbial profiles from HGPS children were compared with microbial profiles of controls from healthy individuals (n = 9) and patients with periodontal disease (n = 9). Results: Comparison of microbial compositions of HGPS samples with periodontal health samples demonstrated significant differences for two bacterial taxa; Porphyromonas catoniae and Prevotella oulora were present in children with HGPS, but not normal controls. There were statistically significant differences of 20 bacterial taxa between HGPS and periodontal disease groups. Conclusions: Typical periodontal pathogens were not present at sites with gingival recession in HGPS children. The microbial compositions of sites of gingival recession and attachment loss in HGPS were generally more similar to those of periodontal health than periodontal disease. Species other than typical periodontal pathogens may be involved in this recession.