ICCBH2017 Invited Speaker Abstracts (1) (1) (2 abstracts)
1Lifecourse Epidemiology Unit, University of Southampton, Southampton, UK; 2NIHR Southampton Nutrition Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust, Southampton, UK.
Peak bone mass is a major determinant of osteoporosis risk and subsequent fragility fractures in older age. There is a wide range of factors influencing peak bone mass, ranging from those acting very early in life, for example in utero and periconception, to those acting through childhood and adolescence into young adulthood. In this presentation I will give an overview of some overarching themes and principles of relevance to peak bone mass, using specific clinical scenarios to illustrate key points. Bone mass increases through growth in childhood to a peak in young adulthood, with the age of peak bone mass varying by individual bone site. Influences on peak bone mass are many and varied, and include common factors which have a small individual contribution, and act at the level of the population, for example nutrition, physical activity, smoking and alcohol intake. The biggest individual effects come from illnesses; almost any severe childhood illness may have an adverse influence on growth. Longer term effects of chronic or repeated illness may result in linear growth failure and/or deleterious effects on bone accrual. One of the key principles in the assessment of bone mass in childhood disease is to differentiate between linear growth failure and a specific adverse effect on bone. The clinical scenarios have been chosen to illustrate several important mechanistic points, of relevance to clinical assessment and treatment, and will include those of chronic inflammation associated with diseases such as Crohns disease and inflammatory arthritis, malabsorption through inflammatory bowel disease and coeliac disease, associations with physical activity in terms of trauma and effects on bone, and hormonal issues such as amenorrhea and weight loss. Acute lymphoblastic leukaemia serves as an example of a disease and its treatment both having negative effects on bone quality. Finally I will consider the increasing evidence for the role of environmental factors in utero, such as maternal gestational 25(OH)D concentration, on long term bone development and potential underlying mechanisms. The clinical implications of the issues discussed will be considered, together with important principles in the assessment of bone mass in children.
Disclosure: N Harvey has received consultancy, lecture fees and honoraria from Alliance for Better Bone Health, AMGEN, MSD, Eli Lilly, Servier, UCB, Shire, Consilient Healthcare and Internis Pharma.