Fracture Repair: Its Pathomechanism and Disturbances

Abstract

Healing of the bone fracture is a biological process that is based on various cell lineages recruited, activated and regulated by molecular mediators, namely chemokines, growth factors, and cytokines, cooperating in a cascade of events aimed to fill the fracture gap with callus. Remodeling of the callus rebuilds the microarchitecture to the mature bonecancellous or compact, depending on the type of the bone that was primarily at the fracture gap. Restitution of the bone continuity requires activation of mesenchymal stem cells that transform into osteoblasts and mature into osteocytes. It is activated and regulated by molecules released from blood platelets from posttraumatic hematoma, traumatized tissues, nerve endings, and inflowing inflammatory cells. The significance of the inflammatory cells in this process is inappreciable, as they eradicate pathogens, remove wound debris, and supply the fracture gap with molecules regulating forthcoming cellular events. They also provide immune regulation of the healing. To proceed uneventfully, healing requires an adequate bone contact and biomechanical environment, proper oxygenation, and nutrition. Unfortunately, up to 15% of bone fractures show some kinds of disturbances that may result in cessation of reparative processes leading to non-union. Factors, responsible for that, are brought to date based on current literature and clinical observations.

Biomaterial and implant induced ossification: in vitro and in vivo findings

“…This causes extravasated blood to form a post‐traumatic hematoma and to cause influx of cells, including inflammatory cells and MSCs. This is then followed by MSC differentiation and release of proteins for ECM deposition (Shiu, Leung, & Ko, 2018; Szcesny, 2018). In the case of the FRC‐BG implant, the inner and outer surfaces of the implant were perforated, which enabled blood penetration and diffusion by capillary forces from the surgical site to cause instant hematoma throughout the implant (Nganga, Ylä‐Soininmäki, Lassila, & Vallittu, 2011b; Nganga, Zhang, Moritz, Vallittu, & Hupa, 2012b).…”

Open versus arthroscopic ankle arthrodesis: A systematic review and meta-analysis

“…In arthroscopic arthrodesis, the soft tissue envelope is disrupted to a minimum degree, which enables the major functions of soft tissues close to the surgical site. The bone healing cascade is activated rapidly, so the bone heals rapidly and function improves in the early stage due to the minimum degree of softtissue envelope disruption [4,23]. The limited exposure causes significantly decreased periosteal stripping.…”

Open versus arthroscopic ankle arthrodesis: a systematic review and meta-analysis

“…In arthroscopic arthrodesis, the soft tissue envelope is disrupted to a minimum degree, which enables the major functions of soft tissues close to the surgical site. The bone healing cascade is activated rapidly, so the bone heals rapidly and function improves in the early stage due to the minimum degree of soft-tissue envelope disruption [4,19]. The limited exposure causes significantly decreased periosteal stripping [20].…”