European journal of pain : EJP
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Chronic pain is pathological, persisting beyond normal tissue healing time. Previous work has suggested ∼50% variation in chronic pain development is heritable. No data are currently available on the heritability of pain categorized using the Chronic Pain Grade (CPG). ⋯ After adjustment, 'any chronic pain' h(2) = 16% (SE 7%; p = 0.02) and 'severe' chronic pain h(2) = 30% (SE 13%; p = 0.007). Co-heritability of both traits was 11% (SE 76%). This study supports the use of chronic pain as a phenotype in genetic studies, with adequate correction for confounders to specifically identify genetic risk factors for chronic pain.
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To clarify the mechanism of tenderness after bone injury, we investigated changes in the withdrawal threshold to mechanical stimuli, nerve distribution and nerve growth factor (NGF)-expression in a rat model of bone injury without immobilization for bone injury healing. Rats were divided into three groups as follows: (1) rats incised in the skin and periosteum, followed by drilling a hole in the tibia [bone lesion group (BLG)]; (2) those incised in the skin and periosteum without bone drilling [periosteum lesion group (PLG)]; and (3) those incised in the skin [skin lesion group (SLG)]. Mechanical hyperalgesia continued for 28 days at a lesion in the BLG, 21 days in PLG and 5 days in SLG after treatments, respectively. ⋯ Anti-NGF and trk inhibitor K252a inhibited hyperalgesia in the different time course. This study shows that localized tenderness coincides with the bone healing and involves NGF expression and nerve sprouting after bone injury. The findings present underlying mechanisms and provide pathophysiological relevance of local tenderness to determination of bone fracture and its healing.