title: Link between obstructive sleep apnea and increased bone resorption in men.
abstract: The bone metabolic abnormalities in patients with obstructive sleep apnea (OSA) were examined. Severity-dependent increases in the serum/urinary levels of bone resorption markers and their attenuation following continuous positive airway pressure therapy in subjects with OSA provide the first evidence of a link between OSA and abnormal bone metabolism.
  
  
  BACKGROUND
  Hypoxia, microinflammation and oxidative stress, well-known pathophysiological features of obstructive sleep apnea (OSA), are also known to affect bone metabolism. We examined the bone metabolic abnormalities in patients with OSA and also the effects of continuous positive airway pressure (CPAP) therapy on these abnormalities.
  
  
  METHODS
  A cross-sectional and prospective study was conducted in 50 consecutive male subjects visiting a sleep clinic and 15 age-matched control subjects without OSA. Plasma concentrations of IL-1beta, IL-6, TNF-alfa, 3-nitrotyrosine, osteocalcin, bone-specific alkaline phosphatase (BAP), and urinary concentrations of cross-linked C-terminal telopeptide of type I collagen (CTX) were examined before and after 3 months' CPAP in subjects with OSA.
  
  
  RESULTS
  The plasma levels of the cytokines as well as the urinary CTX levels were higher in subjects with severe OSA than in those with mild OSA or control subjects. Significant decrease of the urinary excretion of CTX (before: 211+/-107 vs. after: 128+/-59 microg/mmol/creatinine; p<0.01) as well as of the plasma levels of the cytokines was observed following 3 months' CPAP.
  
  
  CONCLUSIONS
  Severity-dependent increases in the serum/urinary levels of bone resorption markers and their reversal following CPAP in subjects with OSA provide the first evidence of a link between OSA and abnormal bone metabolism.
authors.affiliation: Second Department of Internal Medicine, Tokyo Medical University, 6-7-1 Nishi-Shinjuku, Shinjuku-ku, Tokyo 160-0023, Japan. tomiyama@tokyo-med.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Tomiyama
authors.forename: R
authors.initials: R
authors.lastname: Okazaki
authors.forename: D
authors.initials: D
authors.lastname: Inoue
authors.forename: H
authors.initials: H
authors.lastname: Ochiai
authors.forename: K
authors.initials: K
authors.lastname: Shiina
authors.forename: Y
authors.initials: Y
authors.lastname: Takata
authors.forename: H
authors.initials: H
authors.lastname: Hashimoto
authors.forename: A
authors.initials: A
authors.lastname: Yamashina
mesh_terms: D000328:Adult; D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D015415:Biomarkers / Q000378:metabolism; D001862:Bone Resorption / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control; D003094:Collagen / Q000652:urine; D045422:Continuous Positive Airway Pressure; D016207:Cytokines / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000209:etiology; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D018384:Oxidative Stress; D017286:Polysomnography / Q000379:methods; D020181:Sleep Apnea, Obstructive / Q000150:complications* / Q000628:therapy
chemical_list: D015415:Biomarkers; D016207:Cytokines; D018836:Inflammation Mediators; C461299:urinary N-telopeptide of type I collagen, human; D015675:Osteocalcin; D003094:Collagen; D000469:Alkaline Phosphatase