The Pathogenesis of OSA

Project: National Science and Technology CouncilNational Science and Technology Council Academic Grants

Project Details


The pathogenesis of OSA Obstructive sleep apnea syndromes (OSA) is a prevalent disorder. From the study in United states (NEJM 1993, Young), It is estimated 4% of male and 2 % of female affected by this disorders.With similar methodology, prevalence of OSA in Asians was similar around 2-4% in Korea (AJRCCM Kim) and Hong Kong(Chest 2001, Ip M). The major complications of OSA are cardiovascular events and neurocognitive dysfunction. There are evidences show patients with severe OSA have higher mortality and morbidity than normal population and patients with treatment. Another report published in NEJM in 697 patients that followed 6 years show a higher risk of stroke and cardiovascular events than control population. Two large Cohort studies in United State –the Sleep Heart Health Cohort Study andWisconsin Cohort study reported in several journals such as NEJM, Lancet, and Achieve of Internal Medicine proved that OSA is an independent risk factor of hypertension. Intermittent hypoxia induce the occurrence of oxygen radicals which trigger the cascade of inflammation were proposed in the pathogenesis of OSA with cardiovascular events and hypertension. Endothelial dysfunction induced by these inflammation mediators contributes to the occurrence of atherosclerosis and then cardiovascular complication in OSA. Sympathetic tone fluctuated at night in patients of OSA is another hypothesis on the occurrence of hypertension in patients of OSA. Neurocognitive function such as sleepiness, attention, cognition, memory, and executive function are all reported to be poor in patients of OSA. But in hundreds of study on neurocognitive function in patients of OSA show conflicted data because the problems about study designation, small sample size and non-standardized testing methods in these reports. However, patients of OSA do show problems of cognitive function and improve significantly after treatment. The pathogenesis of OSA is not clearly identified. Caniofacial anomaly, neuromuscular deficiency as well as obesity were the major factors contributed to the pathogenesis of obstructive sleep apnea syndrome (OSA). Although the BMI in Asian population is lower than Caucasian’s, the prevalence of OSA between them is similar. 2-4 % of middle age (30-60 years old) Americans suffered from OSA.Whereas the reports from Hong Kong and Korea noted the prevalence of OSA in Asian population is around 3-4%. It means that the pathogenesis of OSA between Asians and Caucasians could be different. The treatment of OSA is not satisfied by patients and physician so far. Low compliance is noted in patients treated by CPAP. Acceptability is better for patients who receive oral appliance, but it mostly was suggested in mild to moderate OSA for the advancement of lower jaw is low. Several methods of surgery is not widely accepted either due to low successful rate in UPPP or high invasiveness by mandible advancement. The low treatment satisfaction rate may largely due to the complexibility of the pathogenesis in OSA. The different factors in the pathogenesis of OSA may take different percentage for the development of OSA in different patients. In Asians population, these pathogenetic factors may totally different from Caucasians. So, it is worthwhile to established a well designed cohort data in Taiwan as the evidence now show the pathogenesis of Asian population are different from Caucasians. As authors mention above, the prevalence rate in Asians countries is similar to Caucasians, but the BMI is much lower in Asians population. The major factors in the pathogenesis of Asians population could be different in Asians population. It could be the different craniofacial factors or neuromuscular or respiratory control. A predictive model will developed using regression analysis for all these variable in the patients of OSA. A better treatment modality could be developed by the predictive model base on the variables.

Project IDs

Project ID:PC10007-1192
External Project ID:NSC100-2314-B182-044
Effective start/end date01/08/1131/07/12


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