74 Theories and techniques of oral implantology

forces migration toward a less compressed area. On the side of degeneration, both the epithelial rests within the periodontal ligament and the epithelial attachment proliferate and occupy that area in which the collagen fibers were destroyed. When the epithelial attachment separates from the tooth's surface, a deep pocket suddenly appears. This usually collects debris, and periodontosis becomes superimposed with periodontitis.

The treatment of periodontosis is difficult, and both systemic and local measures are initiated. The irritants are scaled, the pocket surgically removed, and the loose teeth splinted. Existing occlusal trauma is also eliminated.

SUPPORTING TISSUES OF AN ENDOSSEOUS IMPLANT

An endosseous implant is a foreign body inserted into tissues previously occupied by a natural tooth or teeth. The reactions of these tissues to the introduction of an implant is not the only consideration, for it has been known for years that metallic inclusions are well tolerated by the body. What differentiates the dental implant from other metallic inclusions is the fact that it protrudes into the oral cavity, or out-side the body, and that it is inserted to perform a specific prosthodontic function—to act as an abutment for a fixed denture. How well it serves its intended use depends to a large extent upon the effect it has upon its supporting tissues.

As will be demonstrated here and in other chapters, several current endosseous implant designs are both biologically and mechanically compatible with their supporting tissues. From the moment of insertion they cause little disruption of the normal activities of the site. They not only are not harmful but are actually beneficial in that they re-store functional stimulation to their surrounding tissues. Here the discussion centers on changes in the periodontal tissues caused by an implant, from the trauma inflicted by its insertion to the healing pat-terns characteristic of an implant-occupied site.

Healing of an implant site

The mandible and maxillae are membrane bones, which are said to heal without cartilaginous callus formation. As an implant intervention is performed, the following events occur. Cells forming the oral epithelium and its blood and nerve supply are crushed, the periosteum is severed, and the haversian systems and the circumferential and interstitial lamellae are affected. Osteocytes in the area are

crushed and destroyed. Also, osteocytes in neighboring areas whose processes lie in canaliculi reached by the various drilling tools are also destroyed as their processes are ruptured. The rupturing prevents nutrients, oxygen, and waste products from being circulated to and from cells up to several cells away from the site of injury. These cells, therefore, must disintegrate.

In the injured and dying cells, the production and release of autolytic enzymes takes place. Leukotaxine, a crystalline protein enzyme, is released from the dead cell area and attracts white blood cells. The body temperature rises as pyrotoxin and necrosin are released into the bloodstream, and the blood vessel walls expand, permitting the release of white blood cells. These line up around the site of inflammation.

At the same time, blood that has flooded the area and surrounded the implant itself coagulates, laying down a network of fibrin. The clot closes the openings of injured vessels in the area of the implant, preventing continuous bleeding, and protects the exposed surface of the bony socket. The implant site proceeds to heal as long as the clot holds up. If the clot fails to form or is removed too early—as may occur with a loose-fitting implant--a painful condition known as dry socket occurs. In dry socket, areas of denuded alveolar bone necrotize and are slowly eliminated by undermining resorption.

The orifice around the implant closes after the epithelium fills in across the small opening surrounding it. Until it closes, the cleansing action of saliva helps keep the area free of infection. Once closed, infectious agents can no longer penetrate the site.

Proliferating cells of young connective tissue invade the clot and differentiate. At the base of the implant dense fibrous tissue forms and gradually ex-tends upward to join epithelial tissue that has invaginated about 2.5 mm. The encapsulation of the implant by fibrous tissue is important and beneficial for two reasons. First, bone itself cannot fuse directly to metal, so the connective tissue separates the two elements. Second, the connective tissue acts as a suspensor ligament that transmits the occlusal forces brought to bear upon the implant to the surrounding bone.

As some of the connective tissue cells are forming the membrane around the implant, others are differentiating into fibroblasts. These multiply rap-idly while at the same time hypervascularization