Background: Therapeutic approaches to periodontal regeneration in the past have utilized bone replacement grafts, growth factors, barrier membranes, or combinations of these approaches. More recently, enamel extracellular matrix proteins have been introduced to stimulate periodontal regeneration. One factor thought to have an impact on the outcome of the regenerative process is the initial size of the periodontal defect. This is particularly the case when using proteins to stimulate regeneration, because the concepts of guided tissue regeneration emphasize the need for space maintenance to allow for selected cell repopulation. The goal of this study was to evaluate periodontal regeneration in intrabony defects of various sizes treated with enamel matrix proteins.
Methods: Periodontal defects ranging in size from 1 to 6 mm were created bilaterally around 3 teeth in the mandibles of baboons. Plaque was allowed to accumulate around ligatures placed into the defects. After 2 months, the ligatures were removed, the teeth were scaled and root planed, and a notch was placed at the base of the defect. On one side of the mandible, neutral ethylene diamine tetracetic acid and enamel matrix proteins were used to treat the defects. The other side served as a control, with neutral ethylene diamine tetracetic acid treatment alone after scaling and root planing. Flaps were sutured and the animals were allowed to heal without oral hygiene procedures. After 5 months, the animals were sacrificed and the teeth were processed for histological evaluation.
Results: Periodontal regeneration occurred in all sizes of the periodontal defects. Qualitatively, new cementum, periodontal ligament with Sharpey's fibers, and new bone tissue were observed. In general, enamel matrix protein treatment resulted in greater tissue formation than controls. In many instances, dramatic tissue formation occurred far coronal to the base of the defects. In addition, horizontal bone fill occurred in defects that were initially 4 or 6 mm wide. The resultant width of the periodontal ligament was similar in all defects regardless of the original defect width. The cementum width was slightly greater in the wider (4 and 6 mm) defects compared to the more narrow (1 and 2 mm) defects. When evaluating the combined 1 and 2 mm defects, the height of new cementum with enamel matrix protein treatment was 45% greater than the control, with 31% greater new bone height versus the control. In the combined wider defects (4 and 6 mm), new tissue height was more similar between enamel matrix protein-treated defects and control defects. The results from the wider defects must be interpreted cautiously, because the interproximal bone heights were resorbed more adjacent to the wider defects during the plaque accumulation period and likely limited the potential for regeneration.
Conclusions: The treatment of various sized periodontal defects with enamel matrix proteins stimulated substantial periodontal regeneration. In many cases, dramatic amounts of new cementum, Sharpey's fibers, periodontal ligament, and bone tissue were formed far coronal to the notch at the base of the defect, especially considering the width of the original defects. This periodontal regeneration occurred in the absence of exogenous growth factors, bone replacement grafts, barrier membranes, or their combination.