Wound Healing and Regeneration—Possibilities

The paradigms of periodontitis therapy have changed markedly in the past two decades, due primarily to a veritable flood of new knowledge from medical specialties (McCulloch 1993, McGuire 1996, TenCate 1997, Wikesjö & Selvig 1999, Cho & Garant 2000).

New insights into the guidance and feedback mechanisms of cellular function now permit us to influence the healing processes (Bartold & Narayanan 1998, Christgau 2001, Hägewald 2002). As a result of advances in cell biology, we can better interpret the behavior of the tissues (Amar & Chung 1994, Selvig & Wikesjö 1999). For example:

• The bone-inducing capacity of demineralized bone matrix (proteins such as BMP; Jepsen 1996, Jepsen & Terheyden 2000).

• Concepts of conditioning the nonvascular root surface (acids, Emdogain; Selvig et al. 1988, Trombelli et al. 1995, Hammarström 1997, Blomlöf et al. 2000)

• The “bioacceptability” of a formerly LPS-saturated root surface following detoxification

• The concept of tissue “compartments”; this lead to the GTR technique, because cells colonize the surface according to the principle of “first come—first served” (Fig. 448 B)

• The systemically-modulated, complex and overall active local network of growth factors and differentiation factors, signal molecules and adhesion molecules (Marx et al. 1998, Anitua 2001, Kübler & Würzler 2002)

• The existence of pluripotent stem and precursor cells within the blood stream and in the perivascular tissues.

Despite these enticing new developments and theories, periodontitis therapy today is guided by a strict anti-infectious, anti-microbial concept (Slots et al. 1999), with protocols for the individual treatment techniques. But still lacking are guidelines for the immediate postoperative period, that is during the first phase of healing, for wound care, immobilization and pharmacomechanical plaque control of the healing wound. Stabilization, especially the stabilization of the coagulum, is one of the most important measures. Stabilization mechanisms (adhesins etc.; Somerman et al. 1987, MacNeil & Somerman 1999, Somerman 2001) on the conditioned root surface prevent the downgrowth of epithelium and enhance the secure stabilization of the fibrin matrix. This serves as a natural guidance mechanism for the immigration of factor-guided future tissue cells during the second phase of wound healing.

Periodontal Wound Healing—Definitions

Histologic studies of wound healing have clarified whether and to what extent healing of the gingival and periodontal attachment apparatus is possible in the form of re-attachment or regeneration (Schroeder 1983, Polson 1986, Karring 1988). One differentiates among:

Histologic Terminology

Regeneration—Restitutio ad integrum

Complete regeneration of form and function: Gingiva with junctional epithelium and gingival connective tissue; periodontium with cementum, periodontal ligament, bone.

Repair

Restoration of the continuity in the wound or defect area, without regeneration of the originally intact tissues’ form and function: e.g., long junctional epithelial attachment.

“New Attachment”

New connection of connective tissue with the formerly pathologically exposed root surface, i.e., formation of new cementum with inserted periodontal ligament fibers (also, formation of new bone with Sharpey’s fibers embedded).

Re-attachment

Re-attachment is the re-establishment of the bond between connective tissue and the remaining vital tissue components on the root surface, e.g., cementum and remnants of the periodontal ligament (usually in the deepest areas of the pocket; “dark blue” in Fig. 447/448 C–G).

Note: Epithelial re-attachment does not occur. Epithelium is always established by new cells from the basal cell layer.

Alveolar Bone—“Bone Fill”

Filling a periodontal osseous defect does not provide evidence for complete periodontal regeneration (including newly formed cementum). This can only be demonstrated histologically (Listgarten 1986).

Clinical Terminology

For precise definitions of probing depth, clinical attachment level etc., see “Diagnosis” (p. 165).