The events involved in osseous wound healing around implants recapitulate the events of wound healing which is depicted in the flowchart.
The effect of many inflammatory mediators, eicosanoids, interleukins and is it chemokines on bone formation and osteoblast behaviour in culture strongly implicates the implication of post surgical inflammatory processes in determination of bone formation.After the establishment of a well vascularised, immature connective tissue,osteogenesis continues by the recruitment, proliferation and differentiation of the osteoblastic cells. Differentiated osteoblast secretes a collagenous matrix and contributes to its mineralization.
Eventually during the formation, the matrix surrounds the osteoblastic cells and mineralization of a collagenous rich matrix is completed. This cell rich and unorganized bone is called woven bone. The transformation of woven bone to lamellar bone i.e. bone organized to resist physical strain and displaying a haversian architecture, is another important part of osseointegration. Thus, osseointegration involves the direct bone apposition on the implant surface followed by the structural adaptation of the bone to mechanical load and represents a lifelong process of bone formation, adaptation to function and repair of bone.
Physiologic Adaptation
Modeling is a surface specific activity (apposition or resorption) that produces a net change in the size and/or shape of the bone. It is an uncoupled process meaning that cell activation (A) proceeds independently to formation (F) or resorption (R).Modeling is the fundamental mechanism of growth, atrophy and re-orientation.Remodeling is defined as the turnover or the internal reconstructing of previously existing bone. It is a coupled tissue phenomenon. Activation of the precursor cells results in the following:
The effect of many inflammatory mediators, eicosanoids, interleukins and is it chemokines on bone formation and osteoblast behaviour in culture strongly implicates the implication of post surgical inflammatory processes in determination of bone formation.After the establishment of a well vascularised, immature connective tissue,osteogenesis continues by the recruitment, proliferation and differentiation of the osteoblastic cells. Differentiated osteoblast secretes a collagenous matrix and contributes to its mineralization.
Eventually during the formation, the matrix surrounds the osteoblastic cells and mineralization of a collagenous rich matrix is completed. This cell rich and unorganized bone is called woven bone. The transformation of woven bone to lamellar bone i.e. bone organized to resist physical strain and displaying a haversian architecture, is another important part of osseointegration. Thus, osseointegration involves the direct bone apposition on the implant surface followed by the structural adaptation of the bone to mechanical load and represents a lifelong process of bone formation, adaptation to function and repair of bone.
Physiologic Adaptation
Modeling is a surface specific activity (apposition or resorption) that produces a net change in the size and/or shape of the bone. It is an uncoupled process meaning that cell activation (A) proceeds independently to formation (F) or resorption (R).Modeling is the fundamental mechanism of growth, atrophy and re-orientation.Remodeling is defined as the turnover or the internal reconstructing of previously existing bone. It is a coupled tissue phenomenon. Activation of the precursor cells results in the following:
- Activation (A)
- Resorption (R)
- Quiescence or reversal (Q)
- Formation (F)
The duration of A - R(Q) - F remodeling cycle is also referred to as the SIGMA CYCLE. It is about 6 weeks in rabbits, 12 weeks in dogs and 17 weeks in humans.
Healing Events around Implants
Healing of an implant is compared with the processes in normal bone healing or bone regeneration and with stable osteosynthesis.
The healing events are described in 3 stages
Stage 1: Wound healing and formation of woven bone (callus) (2 to 6 weeks)
Stage 2: Lamellar compaction and remodeling (6 to 18 weeks)
Stage 3: Maturation and adaptation: (18 to 54 weeks)
Stage 1: Wound healing and formation of woven bone (callus) (2 to 6 weeks)
The ability of the body to respond to the “trauma” induced by implantation will influence the kind of tissue response (and hence the degree of integration). Therefore proper surgical handling of the tissues with minimal generation of heat (<47o C for 1 minute or less) during preparation of the surgical site will provide the most predictable healing response.
Healing Events around Implants
Healing of an implant is compared with the processes in normal bone healing or bone regeneration and with stable osteosynthesis.
The healing events are described in 3 stages
Stage 1: Wound healing and formation of woven bone (callus) (2 to 6 weeks)
Stage 2: Lamellar compaction and remodeling (6 to 18 weeks)
Stage 3: Maturation and adaptation: (18 to 54 weeks)
Stage 1: Wound healing and formation of woven bone (callus) (2 to 6 weeks)
The ability of the body to respond to the “trauma” induced by implantation will influence the kind of tissue response (and hence the degree of integration). Therefore proper surgical handling of the tissues with minimal generation of heat (<47o C for 1 minute or less) during preparation of the surgical site will provide the most predictable healing response.
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| Histology of bone formation: WB = woven bone, MA = bone marrow, M = muscle. |
After the formation of initial clot around the surgical site, a minor inflammatory response occurs which includes the proliferation and differentiation of numerous phagocytes and undifferentiated mesenchymal cells from the adjacent periosteum.The ability of the tissues to differentiate will depend on the presence of an intact vascular bed that provides adequate oxygenation for bone differentiation.With the initial placement of the implant, a thin (about 0.5mm) layer of bone in the prepared site will become necrotic from the process of forming the implant site. This bone is replaced by the body as integration proceeds. Initially, an in growth of vascular loops will occur at the rate of 0.5mm per day followed by initial woven bone formation in the first two weeks after initial surgical implant placement. Due to the inert nature of the oxide surface, newly differentiating osteoblastic cells derived from the adjacent periosteum synthesizes woven bone matrix that provides initial bone contact with the oxide surface.
Stage 2: Lamellar compaction and remodeling (6 to 18 weeks)
A remodeling phase is initiated in which hematopoietic-derived osteoclastic cells form cutting cones will remove the established woven matrix (at a rate 40 μm perday). An osteogenic front of lamellar bone differentiation occurs where newly differentiated osteoblasts lay down a mature haversian bone system. This process is influenced by environmental factors such as micro movements of the interface, local vascular supply, and systemic and local release of matrix regulating growth factors. In time, the space between the implant and the bone heals with new bone by a reparative osteogenesis, referred to as creeping substitution, resulting in the clinical fixation of the implant.To maintain sufficiently strong bone implant fixation for post-operative load bearing, it is important to preserve adequate primary implant stabilization and prevent overloading of the newly generated bone that offers secondary support during this interfacial remodeling. This seems to be the only explanation for the fact that maxillary implants are generally granted a much longer unloaded healing phase.
Stage 3: Maturation and adaptation: (18 to 54 weeks)
The final stage involves maturation and adaptation of the implant-bone interface, peri-implant bone and the entire implant supporting skeletal element. This process continues for years or during entire lifetime of implant. Remodeling is influenced by mechanical, metabolic and age related factors. The excess endosteal and periosteal callus is resorbed and stronger bone structures develop in regions under higher strain. If remodeling is not stimulated by loading, or if the rate of bone formation decreases with age, a negative turnover in bone mass just as in osteoporosis is the result.After excessive interfacial remodeling (due to increased resorption or reduced formation of new bone), the bone-implant contacts can not withstand overloading, and direct bone-implant apposition is prevented by relative motion of the implant.As in inadequate primary implant stabilization during initial healing phase or during premature overloading, a layer of fibrous connective tissue develops around the implant. This resultant peri-implant radiolucency indicates the first sign of implant loosening.
Stage 2: Lamellar compaction and remodeling (6 to 18 weeks)
A remodeling phase is initiated in which hematopoietic-derived osteoclastic cells form cutting cones will remove the established woven matrix (at a rate 40 μm perday). An osteogenic front of lamellar bone differentiation occurs where newly differentiated osteoblasts lay down a mature haversian bone system. This process is influenced by environmental factors such as micro movements of the interface, local vascular supply, and systemic and local release of matrix regulating growth factors. In time, the space between the implant and the bone heals with new bone by a reparative osteogenesis, referred to as creeping substitution, resulting in the clinical fixation of the implant.To maintain sufficiently strong bone implant fixation for post-operative load bearing, it is important to preserve adequate primary implant stabilization and prevent overloading of the newly generated bone that offers secondary support during this interfacial remodeling. This seems to be the only explanation for the fact that maxillary implants are generally granted a much longer unloaded healing phase.
Stage 3: Maturation and adaptation: (18 to 54 weeks)
The final stage involves maturation and adaptation of the implant-bone interface, peri-implant bone and the entire implant supporting skeletal element. This process continues for years or during entire lifetime of implant. Remodeling is influenced by mechanical, metabolic and age related factors. The excess endosteal and periosteal callus is resorbed and stronger bone structures develop in regions under higher strain. If remodeling is not stimulated by loading, or if the rate of bone formation decreases with age, a negative turnover in bone mass just as in osteoporosis is the result.After excessive interfacial remodeling (due to increased resorption or reduced formation of new bone), the bone-implant contacts can not withstand overloading, and direct bone-implant apposition is prevented by relative motion of the implant.As in inadequate primary implant stabilization during initial healing phase or during premature overloading, a layer of fibrous connective tissue develops around the implant. This resultant peri-implant radiolucency indicates the first sign of implant loosening.
In this era of molecular medicine, the cellular and molecular activities that underlie the process of osseointegration deserve detailed consideration. These activities are potential targets to improve the rate and quality of bone formation at implant and surgical interfaces.
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