Roger Peynegre

Radiofrequency Is a Safe and Effective Treatment of Turbinate Hypertrophy

Objective To evaluate the safety and efficacy of radiofrequency for reduction of inferior turbinate volume.

Myofibroblast accumulation induced by transforming growth factor-β is involved in the pathogenesis of nasal polyps

Myofibroblasts that express α‐smooth muscle actin(α‐SMA) are detected in many chronic inflammatory diseases. Transforming growth factor‐β (TGF‐β) is a potent inducer of myofibroblast accumulation in tissues. In this study, scattered myofibroblasts and TGF‐β were quantified and localized in nasal polyps (NPs) and normal nasal mucosa(NM). NPs were sampled in 16 patients during ethmoidectomy and NM was obtained from 10 control subjects during rhinoplasty. α‐SMA and TGF‐β were detected using immunohistochemistry and the numbers of labeled cells were quantified (α‐SMA and TGF‐β indices) and compared between NPs and NM. In eight NPs, in which the pedicle was preserved, α‐SMA and TGF‐β were evaluated and compared in the pedicle, central, and tip areas. Finally, TGF‐β expression was compared between low (zone 1), moderate(zone 2), and high (zone 3) zones of α‐SMA positivity. α‐SMA and TGF‐β indices were significantly higher in NPs than in NM. In the eight selected NPs, α‐SMA‐positive cells were significantly more abundant in the pedicle than in the central and tip areas, whereas TGF‐β‐positive cells were significantly more numerous in the pedicle than in the tip area. The number of TGF‐β‐positive cells was significantly higher in zone 3 than in zone 1 of α‐SMA positivity. Myofibroblasts, which are abundant in NPs but rare in NM, could be involved in the growth of NPs by inducing extracellular matrix accumulation. The local development of myofibroblasts in NPs could be controlled by TGF‐β, locally produced by inflammatory cells.

Atypical sinusitis in adults must lead to looking for cystic fibrosis and primary ciliary dyskinesia.

Hypotheses/Objectives: In adults, purulent pansinusitis or nasal polyposis starting early in life or that is permanently infected or associated either with chronic bronchial infection, infertility, or situs inversus are uncommon. In these atypical cases of chronic sinusitis (ACS), a primary dysfunction of the mucociliary clearance can be suspected. Adult patients with ACS were therefore investigated to detect primary ciliary dyskinesia (PCD) or cystic fibrosis (CF).

HLA-DR and ICAM-1 expression and modulation in epithelial cells from nasal polyps.

Objective/Hypothesis Through human leukocyte antigen–DR (HLA‐DR) and intercellular adhesion molecule‐1 (ICAM‐1) expression, nasal epithelial cells could actively participate in the chronic inflammation and eosinophil infiltration observed in nasal polyps. The objective of the study was to evaluate HLA‐DR and ICAM‐1 expression in polyp epithelium and in a culture model of polyp epithelial cells allowing ciliated and secretory differentiation.

Epithelial Cell Proliferation in Nasal Polyps Could Be Up-Regulated by Platelet-Derived Growth Factor†

The modifications of epithelial differentiation and proliferation observed in nasal polyps (NP) could be related to local secretion of growth factors, among which platelet‐derived growth factor (PDGF) could play a key role. We therefore prospectively studied, by immunohistochemistry, proliferating cell nuclear antigen (PCNA, an S‐phase cell marker), PDGF, and CD‐68 (activated macrophages marker) expression in NP and inferior turbinate mucosa (NM) in 11 patients. Our data show that PCNA and PDGF expression are increased in NP epithelium, while CD‐68 expression is increased in NP epithelium and lamina propria when compared to NM. Increased local PDGF secretion by numerous activated macrophages could therefore be involved in epithelial cell proliferation up‐regulation in NP. PDGF could also be involved in the pathogenesis of NP via its connective tissue remodeling actions.