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Histopathological changes after coblation inferior turbinate reduction.

Gilead Berger¹, Dov Ophir, Koby Pitaro

¹Department of Otolaryngology-Head and Neck Surgery, Meir Medical Center, 59 Tchernichovsky St, Kfar Saba 44281, Israel. berger45@netvision.net.il

Archives of Otolaryngology--Head & Neck Surgery

|August 20, 2008

Summary

Coblation inferior turbinate reduction (CITR) causes significant long-term fibrosis and tissue depletion. These changes may impact nasal physiology, warranting further investigation into the effects of this turbinate surgery.

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Area of Science:

Otolaryngology
Histopathology
Surgical Innovation

Background:

Inferior turbinate (IT) hypertrophy is a common cause of nasal obstruction.
Coblation inferior turbinate reduction (CITR) is a surgical technique used for refractory IT hypertrophy.
Histopathological changes following CITR require detailed assessment.

Purpose of the Study:

To evaluate the medium- to long-term histopathological alterations in the inferior turbinate after coblation (cold ablation) inferior turbinate reduction (CITR) surgery.
To compare these changes with those observed after conventional inferior turbinectomy.

Main Methods:

A two-center, prospective, nonrandomized, controlled histological study was conducted.
Histopathological analysis of 22 CITR-treated samples and 18 control (inferior turbinectomy) samples.
Assessment included general features, tissue constituent area fractions, and epithelial integrity.

Main Results:

CITR led to marked fibrosis and depletion of submucosal glands and venous sinusoids in the lamina propria.
Significantly increased connective tissue and decreased submucosal glands/venous sinusoids were observed in the CITR group (P < .001).
Reduced intact epithelium and increased partial epithelial shedding were noted post-CITR (P = .03, P = .04).

Conclusions:

Long-term histopathological effects of CITR include significant fibrosis, glandular and venous sinusoid depletion, and partial epithelial shedding.
Partial epithelial shedding is likely due to vascular damage and reduced epithelial perfusion.
The long-term physiological implications of these CITR-induced histopathological changes remain to be elucidated.