Publication:
Ultrastructural abnormalities of muscle spindles in the rat masseter muscle with malocclusion-induced damage

dc.contributor.authorBani, D.es
dc.contributor.authorBergamini, M.es
dc.date.accessioned2011-05-11T10:57:29Z
dc.date.available2011-05-11T10:57:29Z
dc.date.issued2002
dc.description.abstractHuman temporomandibular disorders due to disturbed occlusal mechanics are characterized by sensory, motor and autonomic symptoms, possibly 1 related to muscle overwork and fatigue. Our previous study in rats with experimentally-induced malocclusion due to unilateral molar cusp amputation showed that the ipsilateral masseter muscles undergo morphological and biochemical changes consistent with muscle hypercontraction and ischemia. In the present study, the masseter muscle spindles of the same malocclusionbearing rats were examined by electron microscopy. Sham-operated rats were used as controls. In the treated rats, clear-cut alterations of the muscle spindles were observed 26 days after surgery, when the extrafusal muscle showed the more severe damage. The fusal alterations affected predominantly capsular cells, intrafusal muscle fibers and sensory nerve endings. These results suggest that in the malocclusion-bearing t rats, an abnormal reflex regulation of the motor activity of the masticatory muscles may take place. They also allow us to hypothesize that muscle spindle alterations might be involved in the pathogenesis of human temporomandibular disorders.es
dc.formatapplication/pdfes
dc.format.extent10es
dc.identifier.issn0213-3911es
dc.identifier.urihttp://hdl.handle.net/10201/20742
dc.languageenges
dc.publisherMurcia : F. Hernándezes
dc.relation.ispartofHistology and histopathologyes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectMuscle spindlees
dc.subjectMasseter musclees
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicinaes
dc.titleUltrastructural abnormalities of muscle spindles in the rat masseter muscle with malocclusion-induced damagees
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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