Altered digit tip blastema differentiation and bone regeneration in skeletally mature Ts65Dn Down syndrome mice.

ABSTRACT: Down syndrome (DS), the result of Trisomy 21 (T21), is associated with accelerated aging and impacts many organ systems across the lifespan, including the musculoskeletal system. Skeletal deficits such as low bone mineral density predispose the T21 population to skeletal injuries, especially as they age, and likely reduce their capacity to repair bone. Previous studies have demonstrated impaired secondary fracture healing in 4-month-old DS mice and diminished bone regeneration in young (2-months-old) DS mice. To investigate how bone regeneration is further impacted in skeletally mature (6-months-old) mice, terminal phalanx (P3) digit tip amputations were performed in a murine model of DS, Ts65Dn mice. The P3 regeneration cascade is characterized by an initial phase of bone degradation foll

SUBMITTER: Wolff SM 

PROVIDER: S-EPMC12693721 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature