Expression of molecular markers for bone formation increases during experimental acute otitis media.
Bony tissues are integral parts of the function of the middle ear and the protection of adjacent vital structures. To explore the reaction of middle ear bone to acute otitis media, rats were challenged with Streptococcus pneumoniae and Haemophilus influenzae. Local changes were monitored for up to 1 month. After reverse transcription, competitive polymerase chain reaction was used to determine the expression levels of two molecular markers of bone formation, osteocalcin and procollagen I, and the two cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha, in the bone. Middle ear bone responded rapidly to bacterial challenge, and the reaction depended upon the causative agent. On day 1, IL-6 and TNF-alpha transcripts were detected in the bone from all middle ears. After a short period of decreased expression of osteocalcin, during which the otitis diagnosis could not be made clinically, the levels of bone formation markers increased dramatically. The maximum levels of these markers were reached on days 6 and 14 for animals challenged with H. influenzae and pneumococci, respectively. Infections induced by pneumococci had a longer duration, and after the initial phase the production of osteocalcin and procollagen transcript were significantly higher in the pneumococcus-infected animals. The results indicate that even in an uncomplicated infection, the bone of the bulla reacts to an acute otitis media with a short period of inhibited osteoblast activity followed by a longer period of new bone formation.
Department of Surgery/Otolaryngology, University of California at San Diego School of Medicine and Veterans Affairs Medical Center, La Jolla, California, USA. asa.melhus@mikrobiol.mas.lu.se
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D000208:Acute Disease; D000818:Animals; D016723:Bone Remodeling / Q000235:genetics / Q000502:physiology; D004195:Disease Models, Animal; D004432:Ear, Middle / Q000382:microbiology / Q000473:pathology; D005819:Genetic Markers; D006192:Haemophilus Infections / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D006193:Haemophilus influenzae; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008297:Male; D015675:Osteocalcin / Q000235:genetics / Q000378:metabolism; D010033:Otitis Media / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D011008:Pneumococcal Infections / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D011347:Procollagen / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D005819:Genetic Markers; D015850:Interleukin-6; D011347:Procollagen; D014409:Tumor Necrosis Factor-alpha; D015675:Osteocalcin