Table 2.
Experimental studies investigating MC appearance and function in fracture healing.
| References | Model | Treatment | Main results |
|---|---|---|---|
| Lindholm et al. (198) | White rats (m/f), tibia fracture | – | Progressive MC accumulation in the periosteal callus; MCs decreased during callus remodeling |
| Lindholm et al. (199) | White rats (m/f), tibia fracture | 17-hydroxy-corticosterone | Progressive MC accumulation in the periosteal callus; delayed healing due to treatment affected MC morphology in size, granulation, and staining |
| Lindholm et al. (200) | White rats (m/f), tibia fracture | Somatotropin and thyrotropin | Progressive MC accumulation in the periostal callus; improved healing due to treatment led to earlier MC accumulation |
| Lindholm and Lindholm (201) | Rabbits (m/f), forearm fracture | – | MCs more abundant in the periosteal callus compared to the endosteal callus |
| Taniguchi (41) | Wistar rats (m), bilateral tibia fracture | – | Few MCs near blood vessels and in the marrow of the early endosteal callus; MCs increase in the late periosteal callus and peak during remodeling |
| Banovac et al. (202) | Sprague-Dawley rats (f), femur fracture | NSAIDs | Few MCs near blood vessels and cartilage of the early endosteal callus; MC accumulation near osteoclastic bone resorption during late remodeling; NSAIDs delayed healing and MC appearance |
| Meyer et al. (203) | Sprague-Dawley rats (f), femur fracture | – | Microarray analysis revealed increased MC marker activity from weeks 2 to 4 after fracture in all age groups |
| Behrends et al. (11) | MC-deficient KitW−sh/W−sh, C57BL/6J mice, femoral cortical window defect | – | Disturbed healing in MC-deficient mice: ↓ Cortical bridging, bone content, endothelial cells, macrophages; ↑ TRAP+ cells |
| Ramirez-GarciaLuna et al. (204) | MC-deficient Cpa3Cre/+ and C57BL/6J mice (m/f), femoral cortical window defect | – | MCs appeared in the connective tissue and marrow of the defect; Disturbed healing in MC-deficient mice: ↓ Cortical bridging, bone content, vascularization, bone mineralization, osteoclasts |
| Kroner et al. (10) | MC-deficient Mcpt-5 Cre+/– R-DTA mice (m), femur fracture | – | MCs increase in the periostal callus near newly formed bony trabeculae and osteoclastic bone resorption sites; Disturbed healing in MC-deficient mice: ↓ Local and systemic inflammation (cytokine release, immune cell recruitment); ↑ bone content; ↓ osteoclastic remodeling |
| Zhang et al. (205) | C57BL/6J, Mcpt-5 Cre YFP, Mcpt-5 Cre iDTR mice (m/f), cranial window defect | rPTH, SC | MC inhibition (SC) and deficiency (Mcpt-5 Cre iDTR): ↑ Healing, ↓ arteriogenesis; rPTH: ↓ MCs in the inflammatory phase by acting on osteoblasts releasing anti-MC factors |
| Hebb et al. (206) | C57BL/6 (m/f), bilateral tibia fracture | – | Microarray analysis revealed increased MC prevalence in younger compared to older mice |