Musculoskeletal tissue engineering: Adipose derived stromal cell implementation for the treatment of osteoarthritis.

Osteoarthritis (OA) is a progressive degenerative joint disease which results in chronic degeneration of articular cartilage and sclerosis of bone. While tendons and ligaments may heal to a limited extent, articular cartilage has poor intrinsic regenerative potential, and critical-sized bone defects and pathological fractures cannot regenerate spontaneously. OA represents a significant burden of disease globally, affecting 240 million people in the world.

Endogenous Mechanisms of Craniomaxillofacial Repair: Toward Novel Regenerative Therapies.

In the fields of oral and craniomaxillofacial surgery, regeneration of multiple tissue types-including bone, skin, teeth, and mucosal soft tissue-is often a desired outcome. However, limited endogenous capacity for regeneration, as well as predisposition of many tissues to fibrotic healing, may prevent recovery of normal form and function for patients. Recent basic science research has advanced our understanding of molecular and cellular pathways of repair in the oral/craniofacial region and how these are influenced by local microenvironment and embryonic origin.

From Chronic Wounds to Scarring: The Growing Health Care Burden of Under- and Over-Healing Wounds.

Wound healing is the largest medical market without an existing small molecule/drug treatment. Both "under-healing" (chronic wounds) and "over-healing" (scarring) cause a substantial biomedical burden and lifelong consequences for patients. These problems cost tens of billions of dollars per year in the United States alone, a number expected to grow as the population ages and the prevalence of common comorbidities ( diabetes) rises.

JUN promotes hypertrophic skin scarring via CD36 in preclinical in vitro and in vivo models.

Pathologic skin scarring presents a vast economic and medical burden. Unfortunately, the molecular mechanisms underlying scar formation remain to be elucidated. We used a hypertrophic scarring (HTS) mouse model in which is overexpressed globally or specifically in α-smooth muscle or collagen type I–expressing cells to cause excessive extracellular matrix deposition by skin fibroblasts in the skin after wounding.