Publications by authors named "S Komarova"
Background: Dental implantation of bone reconstructions in oncologic situations improves patients' orofacial function and quality of life. There are currently no recommendations on the timing of implantation.
Methods: This systematic review with meta-analysis aimed to compare primary and secondary dental implantation of free bone flaps in reconstructions for malignant tumors of the oral cavity.
Bone mineralization is a complex process tightly regulated by both biological factors such as collagen maturation as well as physicochemical factors such as pH. A previous model of biological mineralization captured the biological regulation of bone mineralization dynamics, but not the impact of bone microenvironment such as ion availabilities which may be altered in hypo or hyperphosphatemia. To build an integrated model of bone mineralization, we utilized two previously developed models which addressed a distinct aspect of bone mineralization.
View Article and Find Full Text PDFArticle Synopsis
- * A systematic review identified 23 human studies and 16 animal studies related to osteoclast parameters in OI, analyzing data from 310 patients and 406 OI mouse models.
- * Findings revealed significantly higher collagen degradation markers and osteoclast activity in both patients and mice with OI, with the most notable changes seen in younger patients and those with severe forms of the condition.
Article Synopsis
- Chronic kidney disease (CKD) leads to various health issues, including high phosphate levels (hyperphosphatemia), which can harm blood vessels and cause muscle atrophy.
- In experiments with mice, those with CKD or high phosphate diets showed reduced muscle mass and function, confirming that hyperphosphatemia is linked to muscle damage.
- Direct exposure to high phosphate levels in cultured muscle cells also resulted in muscle atrophy, indicating that high phosphate can independently contribute to muscle injury, particularly in the context of CKD.
Article Synopsis
- Marfan syndrome (MFS) is linked to mutations in the FBN1 gene, affecting fibrillin-1, a protein crucial for bone structure and growth factor regulation, leading to skeletal issues like low bone density and long bone overgrowth.
- A study used a mouse model of MFS to analyze various aspects of bone structure and behavior, including curvature, composition, and mechanical properties across different ages of mice.
- Results indicated that while MFS mice exhibited traits consistent with the syndrome, such as long bone overgrowth and reduced trabecular thickness, their overall mechanical and structural properties were similar to control mice, with some differences in bone matrix crystallinity and porosity.