Age-dependent oral manifestations of neurofibromatosis type 1: a case–control study

Abstract

Introduction Most craniofacial manifestations of neurofibromatosis type 1 (NF1) are considered as a result of tumor compression. We sought to determine salivary changes, caries, and periodontal complications in NF1 patients without tumors in the oral cavity. Objective and methods Eleven NF1 patients without tumors in the oral cavity and 29 matched controls without NF1 were enrolled in this case–control study. Demographic information, medical history, and data of intraoral examinations, including the Decayed, Missing, and Filled Teeth (DMFT) scores and Russel’s periodontal index (PI), were recorded. The functional salivary analysis was performed for sialometry, salivary pH values, and amylase activity. Ingenuity Systems Pathway Analysis (IPA) was conducted to identify mutually activated pathways for NF1-associated oral complications. Results NF1 patients were associated with periodontitis (OR = 1.40, 95% CI = 1.06–1.73, P = 0.04), gingivitis (OR = 1.55, 95% CI = 1.09–2.01, P = 0.0002), and decreased salivary flow rates (OR = 1.40, 95% CI = 1.05–1.76, P = 0.005). Periodontal destruction, salivary changes, and dental caries in NF1 patients were age-dependent. Subgroup analyses based on age stratification suggested that salivary flow rates and salivary amylase activities were significantly low in NF1 patients aged over 20 years and that salivary pH values, PI and DMFT scores were significantly high among NF1- controls aged over 20. All oral complications were not significantly presented in NF1 patients aged below 20 years. IPA analyses suggested that cellular mechanisms underlying NF1-associated oral complications involved chronic inflammatory pathways and fibrosis signaling pathway. Conclusion NF1 patients without tumors in the oral cavity presented a comparatively high prevalence of age-dependent oral complications, including periodontal destruction and salivary gland dysfunction, which were associated with chronic inflammatory pathogenesis.

Bidirectional Relationship Between Osteoarthritis and Periodontitis: A Population-Based Cohort Study Over a 15-year Follow-Up

“…In this first hypothesis, instead of obvious infection and inflammation that develops into septic arthritis (42), periodontal pathogens may cause or aggravate the inflammatory process in the joints, finally developing into osteoarthritis, or even severe osteoarthritis that requires surgical treatment. Apart from being involved in idiopathic or primary osteoarthritis, periodontitis and periodontopathic bacterial invasion (43) have been shown to increase the risk of RA (7,11,17) and DM (5,10,14,18,20,44,45). These clinically evident correlations provide a plausible causal interpretation that may connect periodontitis to secondary osteoarthritis.…”

“…Apart from being involved in idiopathic or primary osteoarthritis, periodontitis and periodontopathic bacterial invasion ( 43 ) have been shown to increase the risk of RA ( 7 , 11 , 17 ) and DM ( 5 , 10 , 14 , 18 , 20 , 44 , 45 ). These clinically evident correlations provide a plausible causal interpretation that may connect periodontitis to secondary osteoarthritis.…”

Exposure to environmental air pollutants as a risk factor for primary Sjögren’s syndrome

“…Canonical Pathway Analysis ( 29 – 32 ) was conducted on Ingenuity Pathway Analysis (IPA) software (QIAGEN, Hilden, Germany) using differentially expressed (DE) RNA-seq data of airway epithelial cells exposed to coarse (n=3), fine (n=3), and ultrafine particulate matter (PM) (n=3) versus control group (n=3) obtained from the National Center for Biotechnology Information-Gene Expression Omnibus database (GEO; GSE7010), as well as parotid gland tissue from patients with pSS (n=3) versus healthy adults (n=3) obtained from GEO (GSE40611). Positive and negative z-scores indicated up-regulation and down-regulation of targeted pathways, respectively.…”

Implications of bacterial plaque in gingival overgrowth induced by orthodontic therapy

“…Gingival overgrowth is a condition with increased incidence, especially in the case of children and adolescents [1]. In the case of children and adolescents, gingival overgrowth predominantly takes the following clinical forms: hereditary gingival fibromatosis [2], gingival overgrowth induced by type I neurofibromatosis [3], but also gingival overgrowth induced by the administration of drugs such as: nifedipine, phenytoin, cyclosporine A [1,4].…”