Skip to content
The process of bone remodeling after bone plate fixation
Bone remodeling after bone plate fixation is an important stage in the later stage of fracture healing, involving the modification of callus and the recovery of bone structure. In the early stage of fracture healing, the primary callus forms, among which the new trabeculae gradually thicken and their arrangement becomes regular and dense. As time goes by, osteoclasts and osteoblasts invade the fracture site, completing the creeping replacement process of dead bone clearance and new bone formation. The original callus is replaced by lamellar bone, forming a strong bony connection at the fracture site. Under the effects of limb movement and weight-bearing, osteoblasts along the stress axis are relatively active, forming more new bone and a strong lamellar bone. Outside the stress axis, osteoclasts are relatively active, absorbing and removing excess callus. Ultimately, the fracture site restored the normal bone structure, leaving no trace histologically and radiologically. The fracture line disappeared and the bone marrow cavity was recanalized.
Influencing factors of bone remodeling
Mechanical force effect: The organism has the ability to change the extracellular matrix under the action of external forces and adapt to the needs of mechanical stress. Integrins and signal receptors are transducers of mechanical action, and mechanical stress can regulate extracellular matrix synthesis or cellular functions. For example, during weightlessness, corresponding changes in bone structure and bone cell function that adapt to the weightless environment occur, manifested as weightless bone loss and osteoporosis; Physical activity has a positive promoting effect on bone mass. Besides increasing bone density, exercise also has adaptive changes in bone structure and plasticity.
Hormones: The growth and remodeling of bones are influenced by various hormones, including growth hormone, thyroid hormone and sex hormones, etc. These hormones play a significant role in bone metabolism, regulating the activities of osteoblasts and osteoclasts, thereby influencing the process of bone remodeling.
Nutrition: The growth and remodeling of bones require sufficient nutrients, including calcium, vitamin D, vitamin C and protein, etc. The intake of protein has a significant impact on peak bone mass. People with protein-energy malnutrition are often accompanied by osteoporosis and increased bone fragility. Insufficient protein intake reduces the production of IGF-1, especially in the years before puberty and maturation, where protein intake has the greatest impact on bone mineral density.
Inflammation: The inflammatory response plays a significant role in the process of fracture healing. After a fracture, inflammatory cells around the bone tissue release some growth factors to promote bone repair and remodeling. However, severe inflammatory responses may also have adverse effects on bone remodeling.
Age: The growth and remodeling ability of bones gradually decline with age. Children have a stronger remodeling ability than adults. During the process of fracture repair, children have the ability to correct residual deformities. This ability not only depends on the bone remodeling mechanism during the fracture healing and remodeling period, but also is related to the repositioning of the growth part of the long bone body caused by asymmetric growth after fracture.
Genetic factors: Epigenetics is involved in the regulatory process of bone formation and can have a significant impact on the differentiation of osteoblasts and osteoclasts. Epigenetics mainly regulates gene expression at three levels: DNA modification, histone modification and non-coding RNA, thereby influencing bone remodeling.
Endocrine hormones and paracrine hormones/growth factors/cytokines: Bone remodeling includes special angiogenesis, collectively known as bone remodeling units (BRCS). The flat cells surrounding them can express OPG and RANKL, etc. The special microenvironment created by BRCS can regulate the activities of osteoblasts and osteoclasts. Meanwhile, there are many paracrine – autocrine hormones (factors) in bone tissue, most of which belong to the category of cytokines and growth factors. They are secreted into the bone microenvironment through bone cells or hematopoietic stem cells via autocrine or paracrine pathways, and interact locally or work together with endocrine hormones to regulate bone metabolism. The roles of cytokines and growth factors on osteoclasts are more important than those on osteoblasts because osteoclasts reside in the humoral microenvironment of bone. The interconnection of bone remodeling, information transmission, and the coupling of osteoclasts and osteoblasts must all be achieved through cytokines.