Asthma is characterized by
inflammation of the airways that includes eosinophils, basal membrane thickening, epithelial sloughing, vascular changes, smooth muscle
hypertrophy and
hyperplasia, and mucous gland
hyperplasia. Recently, there have been studies on the role of
hypersensitivity and
inflammation in
asthma, but the role of bronchial smooth muscle remains unclear.
Bronchial thermoplasty is an endoscopic procedure that is approved by the US Food and Drug Administration (FDA) for the treatment of severe refractory
asthma, based on the local delivery of radio frequency at 65°C to the airways, with the aim of controlling
bronchospasm through a reduction of airway smooth muscle (ASM). Several recent studies have shown significant improvement in clinical outcomes of
bronchial thermoplasty for
asthma, including symptom control, reduction in exacerbation and hospitalization rates, improved quality of life, and reduction in number of working days or school days lost due to
asthma. Data from these recent studies have shown reduction in ASM following
bronchial thermoplasty and changes in
inflammation patterns. It has also been argued that
bronchial thermoplasty may have modulating effects on neuroendocrine epithelial cells, bronchial nerve endings, TRPV1 nerve receptors, and type-C unmyelinated fibers in the bronchial mucosa. This may involve interrupting the central and local reflexes responsible for the activation of
bronchospasm in the presence of
bronchial hyperreactivity. Several questions remain regarding the use of
bronchial thermoplasty, mechanism of action, selection of appropriate patients, and long-term effects. In this review, the role of ASM in the pathogenesis of
asthma and the key aspects of
bronchial thermoplasty are discussed, with a focus on the potential clinical effects of this promising procedure, beyond the reduction in ASM.