title: Analysis of pain in the rabbit temporomandibular joint after unilateral splint placement.
abstract: OBJECTIVE
  To determine whether behavioral, anatomical, and physiologic endpoints widely used to infer the presence of pain in rodent models of temporomandibular disorders (TMD) were applicable to the rabbit model of TMD associated with altered joint loading.
  
  
  METHODS
  Unilateral molar dental splints were used to alter temporomandibular joint (TMJ) loading. Changes in nociceptive threshold were assessed with a mechanical probing of the TMJ region on nine splinted and three control rabbits. Fos-like immunoreacitivty in the trigeminal subnucleus caudalis was assessed with standard immunohistochemical techniques from three splinted and six control animals. Retrogradely labeled TMJ afferents were studied with patch-clamp electrophysiologic techniques from three splinted and three control animals. Remodeling of TMJ condyles was assessed by histologic investigations of three splinted and three control animals. A Student t test or a Mann-Whitney U test was used with significance set at P < .05 to compare splinted to control samples.
  
  
  RESULTS
  While variable, there was an increase in mechanical sensitivity in splinted rabbits relative to controls. The increase in Fos+ cells in splinted rabbits was also significant relative to naïve controls (86 ± 8 vs 64 ± 15 cells/section, P < .05). The rheobase (364 ± 80 pA) and action potential threshold (-31.2 ± 2.0 mV) were higher in TMJ afferents from splinted rabbits compared to controls (99 ± 22 pA and -38.0 ± 2.0 mV, P < .05). There was significant remodeling in the condylar fibrocartilage layers as manifested by a change in glycosaminoglycan distribution and a loss of defined cell layers.
  
  
  CONCLUSIONS
  Behavioral and anatomical results were consistent with an increase in nociceptive signaling in concert with condylar remodeling driven by altered TMJ loading. Changes in excitability and action potential waveform were consistent with possible compensatory changes of TMJ afferents for an overall increase in afferent drive associated with joint degeneration. These compensatory changes may reflect pain-adaption processes that many patients with TMJ disorders experience.
authors.forename: Sarah E
authors.initials: SE
authors.lastname: Henderson
authors.forename: Mauro A
authors.initials: MA
authors.lastname: Tudares
authors.forename: Michael S
authors.initials: MS
authors.lastname: Gold
authors.forename: Alejandro J
authors.initials: AJ
authors.lastname: Almarza
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001862:Bone Resorption / Q000473:pathology; D001933:Brain Stem / Q000737:chemistry / Q000473:pathology; D002358:Cartilage, Articular / Q000737:chemistry / Q000473:pathology; D004195:Disease Models, Animal; D005157:Facial Pain / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006025:Glycosaminoglycans / Q000032:analysis; D008310:Malocclusion / Q000150:complications; D008335:Mandibular Condyle / Q000737:chemistry / Q000473:pathology; D009475:Neurons, Afferent / Q000502:physiology; D059225:Nociception / Q000502:physiology; D017288:Pain Threshold / Q000502:physiology; D018408:Patch-Clamp Techniques; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis; D011817:Rabbits; D013165:Splints; D013314:Stress, Mechanical; D013704:Temporomandibular Joint / Q000294:innervation; D013705:Temporomandibular Joint Disorders / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D014275:Trigeminal Caudal Nucleus / Q000737:chemistry / Q000473:pathology; D012668:Trigeminal Ganglion / Q000737:chemistry / Q000473:pathology
chemical_list: D006025:Glycosaminoglycans; D016760:Proto-Oncogene Proteins c-fos