Periostin and receptor activator of nuclear factor κ-B ligand expression in allergic fungal rhinosinusitis

BackgroundAllergic fungal rhinosinusitis (AFRS) is a disease demonstrating substantial eosinophilic inflammation and characteristic radiographic bony erosion/expansion. Periostin is an extracellular matrix protein associated with eosinophil accumulation in eosinophilic esophagitis, allergic asthma mucus production, and chronic rhinosinusitis (CRS) polyp formation. Receptor activator of nuclear factor -B ligand (RANKL) is an osteoclast activator present in osteoporosis and periodontal disease. We sought to evaluate periostin and RANKL expression in AFRS and correlate these levels with radiographic scales of disease severity. MethodsThirty sinus tissue specimens were intraoperatively collected from 3 patient groups: AFRS; CRS without nasal polyps (CRSsNP); and controls (n = 10 per group). Specimens were analyzed by semiquantitative reverse-transcription polymerase chain reaction (sq-RT-PCR) and immunofluorescence (IF) labeling/confocal microscopy for the presence of both periostin and RANKL. Immunofluorescence staining intensity was quantified by pixel density analysis. Preoperative computed tomography (CT) scans from each patient were scored using both the Lund-Mackay and CT bone erosion scoring systems. ResultsPeriostin was significantly elevated in AFRS sinus tissue compared to CRSsNP and controls, as demonstrated by IF (p < 0.001) and PCR (p = 0.011). RANKL was not detected in sinus tissue by IF or PCR. Periostin levels positively correlated with radiographic indices of disease severity for both soft tissue and bone, using Lund-Mackay (r = 0.926 [PCR] and r = 0.581 [IF]) and CT bone erosion (r = 0.672 [PCR] and r = 0.616 [IF]) scoring systems, respectively. ConclusionPeriostin is increased in AFRS tissue compared to CRSsNP and controls. Periostin levels positively correlate with radiologic disease severity scores. The increased levels of periostin in AFRS are possibly tied to its intense eosinophilic inflammatory etiology.