The discovery ofosseotntegranon in the 1960s forced a reexamination of traditional concepts of wound healing. Before acceptance of these findings it was thought that the body would eventually expel any foreign mate.
rial placed through an epithelial surface. This would occur as the epithelium bordering the foreign material migrated down along the interface with the foreign material, finally fully surrounding the portion of the foreign body protruding into the body, causing the material to be completely external to the epithelial barrier. For a dental implant, this meant eventual loosening
of the implant.
The innate tendency of nonmalignant epithelium to surround and externalize foreign material was thought to be the result of the principle of contact inhibition (discussed previously), whereby any epithelial surface
disrupted by any force or object triggers epithelial growth and migration. The epithelium continues to spread until it contacts other epithelial cells and is inhib
ited from further lateral growth. Investigators found that if an inert foreign material was placed through an epithelial barrier and allowed to develop a biologic bond with surrounding bone, epithelial migration down Into
the bone along the implant surface would be resisted. However, if instead, the implant had an intervening layer of connective tissue between itself and the- bone, epithelium would migrate down the implant, externalizing
it. Thus when an implant integrated with bone (osseointegration), lateral growth of epithelium stopped without contact inhlbitlon, as it was classically concelved tofuncnon (Fig; 4-9).
The reasons why epithelium docs not continue to migrate when it meets a borie and implant interface are still unclear, Nonetheless, dentistry has used this aberration in normal wound healing principles to provide integrated metal posts (implants) that are extremely useful to
stabilize dental prostheses. Surgeons use similar techniques to place implants through skin in other body sites to stabilize prosthetic ears, eyes, noses, and so on.
Wound healing around derital implants involves the two basic factors: (1) healing of bone to the implant and (2) healing of alveolar soft tissue to the implant. Dental implants made of pure titanium are used in the discussion
of healing around dental implants; similar healing occurs around properly placed implants made of other inert materials.
Bone healing onto the surface of an implant must occur before any soft tissue forms between the bone and implant surfaces. Maximizing.the Ilkelihood of bone winning this race with soft tissue to cover the implant
requires the following four factors: (1) a short distance between the bone and implant, (2) viable bone at or very near the surface of the bone along the implant, (3) no movement of the implant while bone is attaching to its
surface, and (4) an implant surface free of contamination by organic or inorganic materials.
A short distance between the bone and compliant depends on preparing.a bony site into which the implant fits precisely. Minimizing bone damage during site prepa
rati~n preserves the viability of bone .near the implant surface. Much of the damage caused by preparing an implarit ‘site is the result of heat from friction during the cutting process.
Limiting heat ‘production and rapidly dissipating the heat created at the site help protect the viability of bone along the cut surface. This is accomplished byusing sharp bone-cutting instruments and limited cutting speeds to minimize frictional heat and by keeping the bone cool with irrigation during site preparation. Additional damage -to the cut surface of bone may occur if the site rll’comes infected. This’ is addressed to some degree by using aseptic surgical techniques; systemic topical antibiotics or both.
Keeping forces off the implant prevents movement along the healing bone and implant interface during the critical portion of the healing period. Countersinking implants and using low-profile healing screws decrease
the ability of any forces to be delivered to the implant.
Covering the top of the implant with gingiva during healing further protects it. Implants that are threaded or otherwise fit tightly into the prepared site are better protected from movement than nonthreaded or loose implants. Eventually, once initial integration has occurred, some limited daily pressure on the implant (1000 urn of strain) will actually hasten cortical bone deposition on the implant surface.
Finallv, the surface to which bone is intended to attach must be free of surface contaminants. Such contaminants include bacteria, oil, glove powder, foreign metals, and foreign proteins. The surface of an implant intended to osseointegrate must not be handled with bare or gloved fingers or forceps made of a metal different from the implant, or have retained machine oil or detergent.
The surface of pure titanium implants is completely covered by a 2000-A-thick layer of titanium oxide. This stabilizes the surface, and it is to this’ oxidized surface that bone must attach for osseointegration to occur.
Regardless of how much care is taken to rmrurmze damage to bone during implant site preparation, a superficial layer oi bone along the surface of a prepared implant site becomes nonviable as a result of thermal and
vascular trauma. Although the living cells in the bone die, the inorganic bone structure remains. Under the influence of local growth factors, bone cells directly underlying this bone structure and blood-borne undiffer-
, entiated mesenchymal cells repopulate and remade the bony scaffold with osteoblasts, osteoclasts, and osteocytes. The nonviable bone is slowly replaced with new, viable cortical bone through the process of creeping substitution. Cutting cones move through the bone at a.rate of 40 1-1I11/day,removing dead bone and ‘leaving new osteoid.
At the implant surface, glycosarninoglycans secreted by osteocytes coat the oxide layer. Soon osteoblasts begin to secrete a layer of osteoid over the proteoglycan layer. Bone then goes on to form if proper conditipris (e.g., no implant movement, good oxygen supply) continue during
the months required for healing. The greater the amount of available implant surface, the greater the amount of implant osseointegration. Thus longer or wider-diameter implants and those with sandblasted rather than polished surfaces have more surface available for osseointegration.
The initial deposition .of bone’ must occur before epithelium migrates onto or fibrous connective tissue forms on the implant surface. If soft tissue arrives first at any part of the implant surface, bone Will never replace
the soft tissue at that site. If too much of the implant surface becomes covered with soft tissue rather than bone, the implant will not become sufficiently osseointegrated to use for a dental prosthesis.
Clinicians have found that in some circumstances they can selectively aid the bone-forming process in its race to cover a surface before soft tissue fills the site. An example of this is the use of woven membranes that have
a pore size adequate’to allow oxygen and other nutrients to reach the .bone “rown beneath the membrane, while • keeping fibroblasts-and other tissue elements outside the membrane. By selectively excluding soft tissues, bone is “guided into a desired position; thus guided-tissue regeneration is the term used to describe this process.
The component of an implant that extends through the oral mucosa also has the ability to alter the contactinhibition process that normally controls closure of openings through epithelium. In this case once oral epithelium reaches the surface of a titanium abutment, it seems to stop migrating and secretes a ground substance that attaches the soft tissue to the metal. A hemidesmosomal, basal lamina system forms, further strengthening soft tissue attaching to the implant abutment.