Osseointegration Flashcards

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0
Q

What is meant by the term “primary stability”?

A

The immediate stability achieved when the artificial implant is mechanical fixed. The implant should be able to withstand axial, rotational and lateral forces.

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1
Q

Define the terms osseointegration and clinical osseointegration.

A

Osseointegration is the direct structural and functional connection between living bone and the surface of a load-bearing artificial implant.
Clinical osseointegration is the process whereby clinically asymptomatic rigid fixation of alloplastic materials is achieved and maintained in bone during functional loading.

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2
Q

Why is primary stability important?

A

It is necessary for clinical success and is required for successful healing by true osseointegration (secondary stability).

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3
Q

What are the two types of bone?

A

Cortical (AKA compact bone)

Cancellous (AKA trabecular or spongy bone)

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4
Q

Which clinical and biological factors affect primary stability?

A

Clinical: implant design, patient factors, surgical technique
Biological: bone quality and bone quantity

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5
Q

How could bone be of poor quality?

A

If it has reduced blood supply and cellularity.

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6
Q

What are the factors that affect primary stability through surgical technique?

A
  1. Placing an implant in as much cortical bone as possible
  2. Reducing the diameter of the osteotomy related to implant diameter
  3. Placing the implant immediately after extraction - good or bad?
  4. Immediate or delayed loading - which is best?
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7
Q

What does “secondary stability” mean?

A

The solid fixation of the implant by osseointegration to enable long-term success of load-bearing.

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8
Q

What happens to the bone and titanium oxide during osseointegration?

A

The bone is laid down very close to the implant without intervening connective tissue -> there is no fibrous tissue laid down to mimic the PDL. Titanium oxide fuses permanently with bone.

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9
Q

What is Branemark’s principle of healing?

A

Branemark suggested that the implant screw itself should be inserted into the bone and left from 3-6 months unloaded and out of function to heal before being loaded ie: the crown is then placed and thereby exposing the implant to masticatory forces.

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10
Q

Describe implications of secondary stability on implant healing.

A

Implant healing is a highly dynamic, continuous process that results in maintenance of peri-implant bone and depends on both bone modelling and remodelling.

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11
Q

What is a defining morphological feature of successful osseointegration?

A

Osteoblasts and mineralised matrix contact the implant surface even when loads are applied. Once fixtures are attached, forces are transmitted to surrounding bone.

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12
Q

What design of implant is more used today and why are they only used in adults?

A

Tapered designs are favoured over cylindrical ones. An implant is like an ankylosed tooth so will not respond to orthodontic movement - PDL is responsible.

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13
Q

What is peri-implant endosseous wound healing?

A

The cascade of molecular and cellular processes that provides for new bone growth and differentiation along the biomaterial surface.

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14
Q

What are the healing phases of peri-implant endosseous wound healing?

A
  1. Osteoconduction
  2. De novo bone formation
  3. Bone remodelling
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15
Q

What is osseoconduction?

A

The first and most important healing phase of endosseous wound healing. It relies on the recruitment and migration of osteogenic cells to the implant surface, through the residue of the peri-implant blood clot.

16
Q

What is de novo bone formation?

A

The second healing phase of endosseous wound healing. It results in a mineralized interfacial matrix equivalent to that seen in the cement line in natural bone tissue. The two healing phases, osteoconduction and de novo bone formation, result in contact osteogenesis and, given an appropriate implant surface, bone bonding.

17
Q

What is bone remodelling?

A

A slow process that continues throughout the life of the implant.

18
Q

What is meant by distance vs. contact osteogenesis?

A

Of the two layers involved in peri-implant wound healing, bone can form on either surface and is a combination of both:
Distance osteogenesis -> bone formation starts on the old bone.
Contact osteogenesis -> bone formation starts on the implant surface.

19
Q

Describe the process of osteogenesis.

A
  1. Activated platelets release a number of growth factors including PDGF, TGFß that are mitogenic for: fibroblasts and osteoblasts; and chemotactic for: fibroblasts, neutrophils and osteogenic cells
  2. Recruitment of multipotent progenitor cells
  3. Progressive differentiation into osteoblasts
  4. Initiation of bone formation
  5. Implant surface is important: potentially modulates level of platelet induction and/or maintains anchorage of fibrin scaffold along which cells must migrate
20
Q

Give examples of growth factors released by activated platelets.
What are they mitogenic and chemotactic for? What do these terms mean?

A

PDGF and TGFß.
Mitogenic (encourages a cell to commence cell division AKA mitosis) for fibroblasts and osteoblasts.
Chemotactic (movement of an organism in response to a chemical stimulus) for fibroblasts, neutrophils and osteogenic cells.

21
Q

What are some key cellular elements required for osseointegration?

A

Monocytes/macrophages; osteoclasts; mesenchymal progenitor cells; osteoblasts; fibroblasts; cells associated with angiogenesis.

22
Q

What type of bone first forms after the initiation of osteoclastogenesis on host bone surface? And when?

A

Woven bone in days 5-7

23
Q

What percentage of osseointegration can be seen under the light microscope level?

A

60-70% of implant surface

24
Q

What percentage of Bone Implant Contact (BIC) can be seen in the maxilla and mandible? What is the clinical relevance for the difference in values?

A

> 50% in maxilla
75% in mandible
Clinical relevance is unknown.

25
Q

What is the percentage difference in Bone Implant Contact (BIC) between loaded and unloaded implants?

A

Unloaded implants have 10% less BIC.

26
Q

Describe the layer of substance between bone and implant as seen under the electron microscope.

A

20-500nm thick layer of dense, amorphous (i.e. NON fibrous) substance between bone and implant of organic bone matrix origin -> probably proteoglycans and possibly osteopontin and bone sialoprotein; it is partly calcified.

27
Q

Outline the methods of clinical assessment of osseointegration.
Are they evidence-based?

A

Radiographs give poor resolution; resonance frequency analysis (RFA) is an objective method for stability testing.
Not evidence-based: largely anecdotal evidence from case reports and without RCTs. From a strictly scientific viewpoint, the effectiveness of dental implants is not proven; observational studies demonstrated great advantages with regard to function, aesthetics and psychosocial factors .

28
Q

Give examples of reasons for failure of osseointegration.

A
  • Poor surgical technique (infection, over-heating of bone, over-instrumentation)
  • Poor design (implant surface factors, shape of implant; overloading due to poor prosthetic design, loading too early)
  • Patient related factors (limited available bone, poor oral hygiene, bruxism, age, smoking, radiotherapy, medications, blood supply of bone)
29
Q

What clinical features signify a failed implant?

A
  • Mobility
  • Pain (nerve bundles close to the implant body)
  • Gingival inflammation
  • Chronic inflammation can lead to long-term recession and peri-implantitis
  • Bone erosion/loss of bone around implants
  • Implant fractures
30
Q

What is the goal of enhancement strategies?

A

To provide enhanced osseous stability through micro-surface mediated events.

31
Q

Summarise the different enhancement strategies aiming to improve the degree of osseointegration.

A
  1. Use of surface topography (distribution of features) to enhance osteoconduction -> manipulation of surface topologies on nanoscale level
  2. Biological means to manipulate the type of cells that grow on the implant surface -> attachment of various ions (calcium, phosphate, magnesium, fluoride) or extracellular components (collagen type I)
  3. Use of the implant as a vehicle for delivery of a bioactive coating that may achieve osteoinduction (bone morphogenic protein BMP-2 inducing bone) along its surface -> modulations of linker sequences to attach the RGD (fibronectin cell adhesion) to metal surface but this could lead to inflammation
32
Q

What is the goal of and the hindrance to surface roughness?

A

Goal: to enhance cell attachment, osteogenic differentiation, cell proliferation and/or cell viability
Hindrance: Reproducible surface roughness on a nanoscale level is difficult to achieve

33
Q

What is the goal of and the hindrance to surface coating with biomaterials?

A

Goal: To coat the implant surface with layers of bioactive molecules
1. to serve as matrices for subsequent osteogenic cell attachment and growth e.g. hydroxyapatite by plasma spraying
2. to increase adhesion e.g. fibronectin, RGD sequence motifs
Hindrance:
1. although superior initial rates of osseointegration have been achieved experimentally, long-term failure caused by delamination of coating and particle release from implant surface occurs
2. no increase in BIC or osteoblast differentiation shown yet. Non-specific adsorption of plasma proteins may also occur together with unfavourable interaction with inflammatory molecules

34
Q

What do bone morphogenic proteins (BMPs) do?

A
  • Enhance osteogenesis
  • Drive multipotent progenitor cells into the osteogenic lineage and promote ECM formation
  • Promote tooth XLA socket healing, PI wound healing and sinus floor and alveolar ridge augmentations
35
Q

What does platelet-derived growth factor (PDGF) do?

A
  • Enhances osteogenesis
  • It is a potent mitogen and chemotactic factor for mesenchymal cells including osteoblasts
  • Regulates vascular endothelial growth factor (VEGF) to promote angiogenesis
    BUT ALSO has been shown to inhibit osteogenesis (may need pulses of exposure rather than continuous delivery.
36
Q

What are some current issues of implant design?

A
  • Majority of implants are still made from titanium (zirconium, tantalum, niobium, hafnium, titanium alloys may also show osseointegration) and ceramic materials such as zirconium dioxide may have adequate implant stability
  • Type of implant: threaded design but NOT a cylindrical design without thread
  • Improvements to implant-bone interface features are always in progress
  • Surgical technique: two stage with loading after 3-6 months vs one stage with rapid loading? XLA of healthy teeth or not?
  • What is the long-term response to the surviving implants with regard to the health of the marginal bone and soft tissues?
  • “car model” attitude detrimental: new implants and surfaces marketed at a rapid rate where risk of secondary failure is sometimes overlooked
  • Controlled clinical studies are costly and resource-demanding
37
Q

What are some questions that a researcher in the field of implants should consider during the development of new implant design?

A
  • Does the technology work?
  • How does the technology work?
  • Does it matter to the patients?
  • Will it do more harm than good?
  • Will the patient accept the new intervention?
  • Is it worth paying for the new intervention?