Pericytes are defined by their location in vivo; the pericyte partially surrounds the endothelial cell of the microvessel and shares a common basement membrane with it. As an integral part of the microvasculature, pericytes play a fundamental role in maintaining local and tissue homeostasis. Current evidence also suggests that pericytes function as progenitor cells capable of differentiating into a variety of different cell types including osteoblasts, chondrocytes and adipocytes. It is now apparent that cells resembling microvascular pericytes, and termed 'pericyte-like' cells, have a widespread distribution in vivo. Pericyte-like cells have been identified in the inner intima, the outer media, and in the vasa vasora of the adventitia of large, medium and small human arteries (1, 2). Moreover, recent studies have suggested that these cells may be responsible, at least in part, for mediating the calcification commonly associated with atherosclerosis (1, 3, 4). In this review, we a) examine the evidence that microvascular pericytes deposit a bone-like mineralised matrix in vitro, b) compare the morphological and biochemical properties of microvascular pericytes, calcifying vascular cells (CVCs) and 'classical' smooth muscle cells (SMCs) isolated from bovine aorta, c) demonstrate that microvascular pericytes deposit a well-organised matrix of bone, cartilage and fibrous tissue in vivo, and d) discuss recent studies designed to gain a better understanding of how pericyte differentiation is regulated.

Background Hypothalamic‐Pituitary‐Adrenal (HPA) axis dysregulation has been implicated in chronic widespread pain (CWP); the hallmark of fibromyalgia (FM). This is the first study to compare HPA axis changes in individuals with CWP and those at high risk of symptom development. Methods We sought to determine differences in morning and evening salivary cortisol levels in FM (n = 19), those at‐risk (n = 20) and pain‐free controls (n = 17). Risk factors included non‐CWP pain, somatic symptoms, illness behaviour and sleep disturbance. We conducted the study in the absence of centrally acting medication, to address limitations of previous research. Results Repeated measures ANOVA revealed significant main effects of group (p = 0.003), and time of day (p = 0.002), with no significant interaction. Cortisol levels were higher in FM (p = 0.027) and at‐risk (p = 0.003) groups, compared to controls, but there was no significant difference between FM and at‐risk groups. The main effect of group remained significant with sleep problems (p = 0.021) and life events (p = 0.007), but was not significant with anxiety (p = 0.076) or depression (p = 0.098) scores as covariates. With sleep problems as a covariate, cortisol levels remained significantly higher only in the at‐risk group (p = 0.017). Conclusions This study indicates elevated salivary cortisol in FM and those at high risk, and identifies anxiety, depression and sleep problems as potential contributing factors. The results shed light on the dynamic relationship between stress, mood and sleep disorders and the brain's resilience to pain. Significance This study examines neurobiological changes in chronic widespread pain and high risk individuals. One strength of the study is the absence of centrally acting medication. We found high salivary cortisol common to Fibromyalgia and those at risk and identified contributing factors. Our results offer insight into the early mechanistic changes underlying Fibromyalgia development and open up possibilities for early diagnosis and prevention.