Received: June 25, 2003
Accepted: September 7, 2003
Prof. Israel Rubinstein, MD

Key Words
Upper airway W Nose W Mediators W Adhesion molecules W
Cytokines W Cardiovascular complications

Abstract
Obstructive sleep apnea syndrome (OSAS) afflicts about 5% of adults in Western countries and is thought to play an important role in the pathogenesis of cardiovascular disorders and diabetes mellitus. Although the etiology of OSAS is uncertain, intense local and systemic
inflammation are present in these patients. In the upper airway, this process may promote oropharyngeal inspiratory muscle dysfunction and amplify upper airway narrowing and collapsibility thereby worsening the frequency and duration of apneas during sleep. The presence of systemic inflammation, characterized by elevated levels of certain potent pro-inflammatory mediators, such as Creactive protein, leptin, TNF-·, IL-1ß, IL-6, reactive oxygen species and adhesion molecules, may predispose to the development of cardiovascular complications observed in patients with OSAS. Treatment with nasal CPAP abrogates, in part, local and systemic inflammation in these patients. Whether therapeutic interventions aimed at abating inflammation could be a useful adjunct in the treatment of OSAS merits further investigation.

Introduction
Obstructive sleep apnea syndrome (OSAS) is defined as repeated episodes of upper airway occlusion during sleep with consequent excessive daytime sleepiness and abnormalities in cardiopulmonary function. It is estimated that up to 5% of adults in Western countries are likely to have undiagnosed OSAS [1]. Anatomic narrowing of the airway, increased collapsibility of the airway tissues, disturbances in reflexes that affect upper airway
caliber and pharyngeal inspiratory muscle function contribute to upper airway occlusion during sleep [2]. Viewed as predominantly a mechanical problem, the present treatment of OSAS is also mechanical, splinting of the airway by external application of positive pressure.
Despite the attractiveness of such a simplistic model, the past decade has seen an explosion of data implicating a role for inflammation in the pathogenesis of OSAS. In
this perspective, we will review some of these data and argue that upper airway and systemic inflammation may, in part, underlie the process of upper airway occlusion and contribute to the clinical manifestations of OSAS and its cardiovascular complications.