Stress Treatment Theorem in Implant Dentistry

Stress Treatment Theorem for Implant Dentistry

Introduction

Dentistry blends science and art, with esthetics emphasizing the art form and implant dentistry focusing on science.
Dental esthetics involves tooth color and shape to improve a patient's smile.
The field can be separated into biologic and biomechanic components:
- General dentists emphasize the biologic aspects of oral health.
- Common complications with natural teeth are primarily biological, such as periodontal diseases and caries.

Complications of Tooth-Supported Prostheses

Failures of tooth-supported prostheses involve both biological and biomechanical factors.
The four most common complications for a three-unit fixed prosthesis are:
- Caries
- Endodontic involvement
- Unretained prosthesis
- Material fracture
Biological complications occur more frequently (11%-22%) than biomechanical ones (7%-10%).

Implant Dentistry

Implant dentistry mainly involves tooth replacement.
Most implant complications relate to implant sciences rather than esthetics.
Unlike natural teeth, implant dentistry has relatively few biological complications.
Direct bone-implant interface development is largely biological.
Surgical implant phases achieve successful interfaces more than 95% of the time, regardless of the implant system.
Biomechanical complications are more common and occur after loading.
Implant failures often occur within 18 months of initial loading, especially in soft bone types (16% failure).
These failures are usually caused by biomechanical factors due to weak bone quality.
Common non-failure complications are also biomechanical:
- Attachment fracture or complication in implant overdentures (30%).
- Removable-prosthesis fracture (12%).
- Abutment or prosthetic screw loosening in implant-supported fixed prostheses, accounting for 34% of prosthetic complications and 40% after 5 years.
- Implant component fracture (2%-4%).
- Implant body fracture (1%-2%).
Mechanical complications are more frequent than biological implant problems.
Complex engineering structures fail at their weakest link, including dental implant structures.

Stress and Treatment Planning

Etiologic factors for implant-related complications center around stress.
Overall treatment plan should:
- Assess the greatest force factors in the system.
- Establish mechanisms to protect the implant-bone-prosthetic system.

Biomechanical Overload vs. Surgical Failure

Reasons for initial implant non-integration:
- Excessive heat during osteotomy preparation.
- Excessive pressure at the implant-bone interface during insertion.
Excessive pressure at insertion is common in dense bone with thick cortical bone.
Micromovement of the implant during interface development can cause surgical failure.
Movement as little as $20$ microns can cause a fibrous interface at a fracture site.
Brunski observed fibrous tissue interface development with more than $100$ microns of dental implant movement.
The original Brånemark protocol used a two-stage surgical approach to avoid undue pressure and implant movement.
Implants were placed at or below the crestal bone region to reduce movement.
Schroeder also suggested an unloaded healing period with implants placed at or slightly above the gingival tissues.
Occlusal forces on interim removable prostheses over healing implants may cause incision line opening and delay soft tissue healing.
These forces can affect marginal bone around the developing implant site, potentially causing micromovement.
Stresses applied to a healing implant increase complication risks.
Experienced surgeons can often achieve rigid fixations after surgical placement (99% of the time).
Surgical component of implant failures is often the lowest risk.

Early Loading Failure

Implants may fail shortly after initial integration.
The implant appears to have rigid fixation initially, but becomes mobile after loading.
Early loading failure is caused by excessive stress on the bone-implant interface.
Isidor and colleagues found that crowns with excessive premature occlusal contacts led to implant failure in monkeys.
In the same study, implants with increased plaque retention but no occlusal loads did not fail, suggesting biomechanical occlusal stress is a greater risk factor than bacterial plaque.
Early loading failure is worse for the clinician due to patient confidence loss, financial issues, and time commitment.
Early loading failure is related to the force applied and bone density around the implants, affecting up to 15% of implant restorations.
Biomechanical overload can cause early implant failure in soft bone types (up to $40$ %).

Impact of Occlusal Overload on Mechanical Components

Screw Loosening

Abutment-screw loosening is the most common dental implant prosthetic complication (up to $33$ %).
The incidence of screw loosening with single implant crowns can be as high as $59.6$ % within 15 years.
Screw loosening may cause crestal bone loss, screw fracture, implant fracture, or implant failure.
Most loosened screws occur in maxillary and mandibular molar areas (∼ $63$ %) and with single implant-crown restorations (∼ $75$ %).
Biomechanical forces are a significant etiologic factor in screw loosening.
Screw tightening elongates the screw, producing tension or preload within the screw joint.
Preload exerts a force that leaves the screw joint in compression and promotes a springlike effect.
Elastic recovery is transferred to the abutment and implant, creating a clamping force.
For a screw to remain tight, the clamping force must be greater than the separating forces.
External joint-separating forces include parafunction, excessive crown height, masticatory dynamics, prosthesis position, and opposing dentition.
Conditions that magnify external forces include cantilevers, angled loads, and poor occlusal designs.
When external joint-separating forces are greater than the clamping force, the screw will become loose.

Implant Component Biomechanical Complications

Materials follow a fatigue curve related to the number of cycles and force intensity.
A high force can cause immediate fracture, while repeated lower forces can also lead to fracture due to fatigue.
Prosthesis screw fracture has a mean incidence of $4$ % and a range of 0% to 19%.
Abutment screws fracture less often, with a mean incidence of $2$ % and a range of 0.2% to 8%.
Metal framework fractures occur in an average of $3$ % of fixed-complete and overdenture restorations, with a range of 0% to 27%.
Implant body fracture has the least incidence (1%).
Prosthetic material complications for fixed prostheses have a 33% rate at 5 years and 67% after 10 years.
Prostheses-related fractures are more common than implant component fractures.
Uncemented restorations often occur when chronic or shear loads are applied to the cement interface.
Cement strengths are weakest in shear loads (e.g., zinc phosphate cement resists 12,000 psi in compression but only 500 psi in shear).
Bone is also strongest in compression and 65% weaker in shear forces.
Evaluation, diagnosis, and modification of treatment plans for stress conditions are crucial.
The implant dentist should identify sources of additional force and alter the treatment plan to minimize their negative effect.

Marginal Bone Loss

Crestal bone loss has been observed around the permucosal portion of dental implants.
It can range from loss of marginal bone to complete implant failure and dramatically decreases after the first year.
Early bone loss forms a V-shaped or U-shaped pattern.
Current hypotheses for crestal bone loss causes:
- Periosteum reflection during surgery.
- Implant osteotomy preparation.
- Microgap position between abutment and implant body.
- Micromovement of abutment components.
- Bacterial invasion.
- Establishment of a biological width.
- Stress factors.
Understanding the causes of marginal bone loss is critical for long-term peri-implant health.
Marginal bone loss affects esthetics by influencing soft tissue height and papilla presence, potentially leading to anaerobic bacteria and peri-implantitis.

Periosteal Reflection Hypothesis

Periosteal reflection causes a transitional change in the blood supply to crestal cortical bone.
Ninety percent of arterial blood supply and 100% of venous return are associated with the periosteum in long bones.
Reflecting the periosteum affects the cortical bone blood supply, causing osteoblast death.
Blood supply is reestablished once the periosteum regenerates.
Composite bone forms to restore original conditions.
Trabecular bone under the cortical bone is also a vascular source.
The periosteal reflection theory would lead to generalized horizontal bone loss, not localized ditching around the implant.
Generalized bone loss is rarely observed at the second-stage uncovery surgery.

Implant Osteotomy Hypothesis

Implant osteotomy preparation can cause early implant bone loss.
Bone is sensitive to heat, and osteotomy causes trauma, creating a devitalized zone around the implant.
A renewed blood supply is necessary to remodel the bone.
The crestal region is susceptible due to limited blood supply and greater heat generation.
If heat and trauma were responsible, the effect would be noticeable at the second-stage uncovery surgery, but this is not usually observed.
Bone often grows over the first-stage cover screw.

Autoimmune Response of Host Hypothesis

Bone loss around natural teeth is primarily bacteria-induced, and occlusal trauma may accelerate the process.
The implant gingival sulcus in partially edentulous patients exhibits similar bacterial flora to natural teeth.
Adell and colleagues found 80% of implant sulcular regions were without inflammation.
Lekholm and colleagues found deep gingival pockets were not associated with crestal bone loss.
Most bone loss occurs in the first year (1.5 mm) and less each successive year (0.1 mm).
Bacteria autoimmune theory cannot explain the marginal bone loss condition when it follows the pattern most often reported.
Threads and porous implant surfaces exposed to bacteria can cause a rapid loss of bone.
Poor hygiene can accelerate bone loss.

Biological Width Hypothesis

Sulcular regions around implants and teeth are similar in many respects.
A fundamental difference characterizes the sulcus base.
Natural Tooth:
- An average biological width of $2.04 mm$ exists between the sulcus depth and the alveolar bone crest.
- Composed of connective tissue (CT) attachment (1.07-mm average) and junctional epithelial attachment (0.97-mm average).
- CT attachment is the most consistent value between individuals.
- Gingival fibers and hemidesmosomes establish direct contact.
- When a crown margin invades the biological width, the crestal bone recedes.
Implant:
- Abutment-to-implant body connection may be compared with a crown margin.
- Berglundh and colleagues observed 0.5 mm of bone loss below the implant-abutment connection within 2 weeks.
- Lindhe and colleagues reported an inflammatory CT extending 0.5 mm above and below this implant-abutment connection.
Different gingival fiber groups are observed around natural teeth and implants, leading to different attachment mechanisms.
James and Keller began a systematic study to investigate the biological seal around dental implants.
Collagenous components cannot adhere to or become embedded into the implant body.
The hemidesmosomal seal only has a circumferential band of gingival tissue for mechanical protection.
The biological seal prevents bacteria and endotoxin migration but cannot constitute a junctional epithelial attachment.
The amount of early crestal bone loss is unlikely to be solely due to remodeling to establish a biological width below an abutment connection.
The crevice between the cover screw and the implant body during initial healing is similar to the abutment-implant connection crevice.
The biological width hypothesis cannot fully explain several millimeters of marginal bone loss observed with one-stage implants.

Occlusal Trauma

Marginal bone loss on an implant may be from occlusal trauma.
Occlusal trauma is defined as an injury to the attachment apparatus from excessive occlusal force.
Karolyi claimed a relationship between occlusion and bone loss in 1901.
Some authors concluded trauma from occlusion is related to bone loss, although bacteria are necessary agents.
Waerhaug stated there is no relationship between occlusal trauma and periodontal tissue breakdown.
Lindhe and colleagues stated that