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Osteointegration of a spinal implant implies both a mechanical and a morphological bond at the bone–implant interface.
The biological process of osteointegration involves three phases: clot formation and initial mesenchymal cell differentiation, initial bone formation, and finally bone remodeling. Implant material composition, surface topography, and surface chemistry influence the biological process of osteointegration.
Titanium implants have excellent biocompatibility and osteointegration. Polyetheretherketone (PEEK) has good biocompatibility and has a similar elastic modulus to bone, but lacks good osteointegration. Surface modification of PEEK implants improves osteointegration.
Implants with a rough surface have superior osteointegration compared with smooth implants. Hydroxyapatite-coated implants also show superior osteointegration compared with uncoated implants.
Osteointegration is defined as “a direct and functional connection between ordered living bone and the surface of a load-carrying implant.” It implies both a mechanical as well as a morphological connection. The sustained mechanical efficacy of spinal implants such as screws, interbody cages, and hooks require stability, without loosening or subsidence. Direct apposition of bone at the implant surface creates the largest possible surface area over which to distribute a repetitive mechanical load. Much of our understanding of the biology of osteointegration comes from work done in the dentistry and orthopedic fields. Factors such as material composition, implant design, surface topography, and chemistry, as well as implant site preparation, are all influential in achieving successful osteointegration. Although it is the goal for spine implants to achieve osteointegration, whether or not this occurs can be difficult to assess. It is also unknown whether or not successful osteointegration is necessary to achieve good clinical outcomes.
There is a complicated biological process that follows placement of an implant, (i.e., a screw), into bone, that has similar mechanisms to fracture healing and bone formation. Osteointegration can be broken down into three phases. The first phase includes initial clot formation around the implant. The fibrin clot acts as a meshwork needed for cell migration, and releases proinflammatory and cell adhesion proteins, such as fibronectin and vitronectin , , ( Fig. 87.1 ). Macrophages and neutrophils arrive at the implant site to remove cellular debris. , ,
The second phase involves mesenchymal cell differentiation and initial bone formation. Mesenchymal cells can differentiate into osteoblasts, chondrocytes, or fibroblasts. , , Successful osteointegration requires the majority of mesenchymal cells to differentiate into osteoblasts. If differentiation favors a fibroblast lineage, a layer of fibrous tissue forms between the implant and bone, which can lead to inflammation, osteolysis, and implant loosening. , , The differentiation process is dependent not only on cytokines and growth factors but also on specific surface characteristics and the material properties of the implant. , , , Osteoblasts start the process of bone formation on the bone surface (distance osteogenesis) and directly on the implant (contact osteogenisis). Osteoblasts then produce a cement line or lamina limitans, which is a layer of protein composed of bone sialoprotein, osteopontin, and proteoglycans that in turn promotes osteoblast recruitment and proliferation. , , , , , ,
The final phase is the remodeling phase. Osteoclasts resorb imperfections in the initial layer of bone and create a complex lacunar architecture required for further bone formation and maturation. , , Surface texture, chemistry, and implant composition play an important role in all three phases of osteointegration.
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