Faculty Bibliography

IMPORTANCE/OBJECTIVE:Preeclampsia is a devastating disease of pregnancy associated with increased risk of fetal and maternal complications. African American pregnant women have a high prevalence of preeclampsia, but there is a need of systemic analyses of this high-risk group regarding complications, etiology, and biomarkers. OBJECTIVE:The aim of this study was to provide a synopsis of current research of preeclampsia specifically related to African American women. EVIDENCE ACQUISITION/METHODS:A comprehensive search was performed in the bibliographic database PubMed with keywords "preeclampsia" and "African American." RESULTS:African American women with preeclampsia were at an increased risk of preterm birth, which resulted in low-birth-weight infants. Intrauterine fetal death among African American preeclamptic patients occurs at twice the rate as in other races. On the maternal side, African American mothers with preeclampsia have more severe hypertension, antepartum hemorrhage, and increased mortality. Those who survive preeclampsia have a high risk of postpartum cardiometabolic disease. Preexisting conditions (eg, systemic lupus erythematosus) and genetic mutations (eg, sickle cell disease in the mother, FVL or APOL1 mutations in the fetus) may contribute to the higher prevalence and worse outcomes in African American women. Many blood factors, for example, the ratio of proteins sFlt/PlGF, hormones, and inflammatory factors, have been studied as potential biomarkers for preeclampsia, but their specificity needs further investigation. CONCLUSIONS:Further studies of preeclampsia among African American women addressing underlying risk factors and etiologies, coupled with identification of preeclampsia-specific biomarkers allowing early detection and intervention, will significantly improve the clinical management of this devastating disease.

OBJECTIVE:Animal models recapitulating post-traumatic osteoarthritis (OA) suggest that subchondral bone (SCB) properties and remodeling may play major roles in disease initiation and progression. Thus, we investigated the role of SCB properties and its effects on load-induced OA progression by applying a tibial loading model on two distinct mouse strains treated with alendronate (ALN). DESIGN:Cyclic compression was applied to the left tibia of 26-week-old male C57Bl/6 (B6, low bone mass) and FVB (high bone mass) mice. Mice were treated with ALN (26 μg/kg/day) or vehicle (VEH) for loading durations of 1, 2, or 6 weeks. Changes in articular cartilage and subchondral and epiphyseal cancellous bone were analyzed using histology and microcomputed tomography. RESULTS:FVB mice exhibited thicker cartilage, a thicker SCB plate, and higher epiphyseal cancellous bone mass and tissue mineral density than B6 mice. Loading induced cartilage pathology, osteophyte formation, and SCB changes; however, lower initial SCB mass and stiffness in B6 mice did not attenuate load-induced OA severity compared to FVB mice. By contrast, FVB mice exhibited less cartilage damage, and slower-growing and less mature osteophytes. In B6 mice, inhibiting bone remodeling via ALN treatment exacerbated cartilage pathology after 6 weeks of loading, while in FVB mice, inhibiting bone remodeling protected limbs from load-induced cartilage loss. CONCLUSIONS:Intrinsically lower SCB properties were not associated with attenuated load-induced cartilage loss. However, inhibiting bone remodeling produced differential patterns of OA pathology in animals with low compared to high SCB properties, indicating that these factors do influence load-induced OA progression.