Temporomandibular disorders (TMD) and irritable bowel syndrome (IBS) are comorbid functional chronic pain disorders of unknown etiology that are triggered/exacerbated by stress. Here we present baseline phenotypic characterization of a novel animal model to gain insight into the underlying mechanisms that contribute to such comorbid pain conditions. In this model, chronic visceral hypersensitivity, a defining symptom of IBS, is dependent upon on three factors: estradiol, existing chronic somatic pain, and stress. In ovariectomized rats, estradiol replacement followed by craniofacial muscle injury and stress induced visceral hypersensitivity that persisted for months. Omission of any one factor resulted in a transient (1 week) visceral hypersensitivity from stress alone, or no hypersensitivity (no inflammation or estradiol). Maintenance of visceral hypersensitivity was estradiol dependent; resolving when estradiol replacement ceased. Referred cutaneous hypersensitivity was concurrent with visceral hypersensitivity. Increased spinal Fos expression suggests induction of central sensitization. These data demonstrate the development and maintenance of visceral hypersensitivity in estradiol-replaced animals following distal somatic injury and stress that mimics some characteristics reported in patients with TMD and comorbid IBS. This new animal model is a powerful experimental tool which can be employed to gain further mechanistic insight into overlapping pain conditions.

Background & Aims-Chronic visceral hyperalgesia is considered an important pathophysiological symptom in irritable bowel syndrome (IBS); previous gastrointestinal inflammation is a potent etiological factor for developing IBS. Although there are several animal models of adult visceral hypersensitivity following neonatal perturbation or acute colonic inflammation, there is no suitable model of post-inflammatory chronic visceral hyperalgesia. The aim of this study was to establish a model of chronic visceral hyperalgesia following colonic inflammation in the rat.

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