While type 1 diabetes mellitus (T1D) accounts for <10 % of all diabetes, studies suggest that the global incidence of T1D appears to be increasing by 2-3 % per year [ 1, 2 ], attributed to a variety of possible immune-modulatory factors which include societal changes in hygiene, infectious exposures, vitamin D defi ciency, and/or infant diets [ 1 ]. Diagnosis of the disease most commonly occurs in the pediatric population [ 3 ], with peaks in presentation occurring at school entry (5-7 years) and puberty (10-14 years) [ 2 ]. In the USA, prevalence of T1D has recently been estimated at 1 in every 433 youth <20 years of age [ 4 ]. T1D is, foremost, a state of insulin defi ciency due to the progressive, predominantly autoimmune-mediated, destruction of pancreatic beta-cells. As such, unlike type 2 diabetes (T2D), insulinopenia, rather than insulin secretory dysregulation, becomes the overriding phenotype of this disease and insulin replacement therapy is a necessity. In the last two decades, however, therapeutic options (insulin analogues, insulin pumps, continuous glucose sensors) [ 5 - 7 ] have advanced tremendously. And, in recent years, the use of insulin-pump therapy, in particular, continues to increase in an effort to more-tightly regulate glycemic control [ 8, 9 ]. Hence, understanding the protracted pathophysiology of adult diabetic bone disease in T1D requires an appreciation of the individual context in which this comorbidity has developed over an individual lifetime. The following pages will review skeletal defi - cits in T1D as they are currently understood, recognizing that the disease phenotype may change in the future, as treatment options continue to improve.
|Title of host publication||Diabetic Bone Disease|
|Subtitle of host publication||Basic and Translational Research and Clinical Applications|
|Number of pages||22|
|State||Published - Jan 1 2016|
ASJC Scopus subject areas
- Medicine (all)