An increasing worldwide obesity epidemics and a number of obesity-related morbidities has brought on the largescale research into associations between adipose tissue and the skeleton and bone metabolism. The results of relevant published studies, conducted in adults and children, are inconsistent: some reports suggest protective role of body fat on skeletal health, whereas others emphasize a detrimental effect of adiposity on bone mineral density (BMD) and bone turnover. The discrepancies may, at least partly, result from differing methodological approaches across studies. During the last decade, a growing body of evidence has emerged, supporting the view of a negative role of obesity in bone mass accrual during growth. Childhood obesity may lead to fragility fractures and may, therefore, predict early development of osteoporosis in adulthood. The adipokines and hormones secreted by adipocytes are substantially responsible for fat-bone interactions. The effects of adipokines, such as leptin, adiponectin, resistin or visfatin, on BMD during growth, bone modelling and remodelling processes appear multidirectional. Although low BMI has become a commonly accepted risk factor of postmenopausal osteoporosis, and high BMI has been perceived to prevent bone loss, several well-designed paediatric studies have clearly shown a paradoxical deleterious impact of obesity and excessive weight gain on bone tissue. Finally, there is significant evidence that chronic low-grade inflammation induced by obesity is the key mechanism of this negative effect of adiposity on the growing skeleton. The aim of this review is to demonstrate updated knowledge concerning complexity of fat-andbone interactions, and to highlight important pathogenic and clinical implications of childhood obesity on bone structure, BMD, bone strength and metabolism.