Osteoblasts (OBs) and adipocytes (APs) share a common mesenchymal ancestor. It is now clear that mesenchymal stem cell (MSC) maturation along the OB lineage comes at the expense of adipogenesis and vice versa. During aging, this balance increasingly favors the formation of APs. Hematopoiesis also slowly declines during the aging process. The role of OB lineage cells in hematopoiesis has been studied, but less is known about how APs regulate hematopoiesis. A few studies have demonstrated a negative relationship between APs and hematopoiesis; however, there is also evidence that brown adipose tissue (BAT) may promote hematopoiesis. This review will examine the current knowledge of how adipogenesis and osteogenesis change with aging and the implications of this changing environment on hematopoeisis.

Food iron and lead absorption were measured simultaneously in 28 subjects by extrinsically labeling three consecutive meals with the radioactive tracers, iron 59-sulfate and lead 203-chloride. Absorption was measured directly in all subjects by whole-body counting and indirectly in 15 subjects by assessing subsequent levels of tracer in blood. Iron status of the subjects ranged from iron deficient to replete, thus providing a wide range of iron absorption. Statistically significant positive correlations were obtained between food-iron and lead absorption measured by whole-body counting and also between the tracer levels of iron and lead in the blood. However, the correlation between the absorption of the two elements was not strong, as evidenced by the fact that only 50% of the subjects who hyperabsorbed iron also hyperabsorbed lead.

Emerging data suggest that megakaryocytes (MKs) play a significant role in skeletal homeostasis. Indeed, osteosclerosis observed in several MK-related disorders may be a result of increased numbers of MKs. In support of this idea, we have previously demonstrated that MKs increase osteoblast (OB) proliferation by a direct cell-cell contact mechanism and that MKs also inhibit osteoclast (OC) formation. As MKs and OCs are derived from the same hematopoietic precursor, in these osteoclastogenesis studies we examined the role of the main MK growth factor, thrombopoietin (TPO) on OC formation and bone resorption. Here we show that TPO directly increases OC formation and differentiation in vitro. Specifically, we demonstrate the TPO receptor (c-mpl or CD110) is expressed on cells of the OC lineage, c-mpl is required for TPO to enhance OC formation in vitro, and TPO activates the MAPK, JAK/STAT, and NFκB signaling pathways, but does not activate the PI3K/AKT pathway. Further, we found TPO enhances OC resorption in CD14+CD110+ human OC progenitors derived from peripheral blood mononuclear cells (PBMCs), and further separating OC progenitors based on CD110 expression enriches for mature OC development. The regulation of OCs by TPO highlights a novel therapeutic target for bone loss diseases and may be important to consider in the numerous hematologic disorders associated with alterations in TPO/c-mpl signaling as well as in patients suffering from bone disorders.

In patients with SLE with ESRD, the dosing strategies for HCQ with regard to potential toxicity and disparities in prescribing patterns need further study.

Study design: Retrospective review of a clinical database. Objectives: To examine treatment modalities of incident appendicular fractures in men with chronic SCI and mortality outcomes by treatment modality. Setting: United States Veterans Health Administration Healthcare System. Methods: This was an observational study of 1979 incident fractures that occurred over 6 years among 12 162 male veterans with traumatic SCI of at least 2 years duration from the Veterans Health Administration (VA) Spinal Cord Dysfunction Registry. Treatment modalities were classified as surgical or nonsurgical treatment. Mortality outcomes at 1 year following the incident fracture were determined by treatment modality. Results: A total of 1281 male veterans with 1979 incident fractures met inclusion criteria for the study. These fractures included 345 (17.4%) upper-extremity fractures and 1634 (82.6%) lower-extremity fractures. A minority of patients (9.4%) were treated with surgery. Amputations and disarticulations accounted for 19.7% of all surgeries (1.3% of all fractures), and the majority of these were done more than 6 weeks following the incident fracture. There were no significant differences in mortality among men with fractures treated surgically compared with those treated nonsurgically. Conclusions: Currently, the majority of appendicular fractures in male patients with chronic SCI are managed nonsurgically within the VA health-care system. There is no difference in mortality by type of treatment.