Bethany A. Herbert

TL;DR: The osteo-immunomodulatory effects induced by A. actinomycetemcomitans are discussed and the catabolic disruption of balanced osteoclast-osteoblast-mediated bone remodeling is dissected, which subsequently leads to net alveolar bone loss.

TL;DR: Rat macrophages transduced with recombinant adenovirus and bone marrow cells of MKP-1 KO mice significantly decreased IL-6, IL-10, TNF-α and chemokine levels, and formed fewer osteoclasts induced by LPS than compared with control group of cells, indicating that MKp-1 is a key therapeutic target to control of inflammation-induced bone loss.

TL;DR: MKP-1 negatively regulates chemokine-driven OC formation and subsequent bone resorption in response to LPS stimulation, providing useful insight into mechanisms potentially leading to the development of therapeutic treatment of periodontal disease.

TL;DR: This proof-of-concept study suggests a novel target using an intraoral RNA interference strategy to control periodontal inflammation, and validated MK2 siRNA specificity and arrested LPS-induced inflammatory bone loss, decreased inflammatory infiltrate, and decreased osteoclastogenesis.

TL;DR: Results indicate that Dusp1(-/-) dOCP form less numerous, significantly smaller and less functional OC compared to WT controls, which supports the idea that MKP-1 signaling is essential in early osteoclastogenesis in response to RANKL-induced signaling.