Abstract
The pathogenesis of fibromyalgia (FM) is not understood. Neuroendocrine factors are thought to be of major importance. Genetic and familial factors also have been suggested. Sister chromatid exchange (SCE) is known to orginate from reciprocal DNA interchange in homologous loci of sister chromatids in the replication process. Although it occurs spontaneously, chemical and physical agents causing DNA damage may increase SCE frequencies.
This study was carried out in 25 non-smoking adults diagnosed as FM according to the American College of Rheumatology 1990 criteria and 20 non-smoking healthy individuals to determine whether the genetic impairment and DNA damage have an effect on pathogenesis of FM by measuring SCE frequencies.
There was a statistically significant difference between SCE frequencies obtained from the patient and control groups (p = 0.04). We suggested that genetic impairment and increased DNA damage may play a role in the pathogenesis of FM.