Cores of bone from healing extraction sites were studied at time intervals of 4, 6, 8, 10, 12 and 16 weeks. The results revealed that between 4 and 8 weeks proliferation of cellular and connective tissue elements occur within the healing socket. Islands of new bone with an osteoid seam surrounded by osteoblasts are present within the connective tissue. From 8 to 12 weeks the bone undergoes maturation and forms a trabecular pattern. Although less pronounced, and osteoid seam is still present and osteoblasts occur in fewer numbers. By 12 to 16 weeks the bony trabeculae are mature with very little osteoid and few osteoblasts. This bone resembles alveolar trabecular bone. Two phases of bony regeneration are apparent from the present study. From 4 to 8 weeks there is a progressive osteogenic phase with proliferation of osteogenic cells and immature bone formation. From 8 to 12 weeks the osteogenesis slows down and the trabeculae mature and increase in volume. From 12 to 16 weeks the bone appears to stabilize with an established alveolar trabecular bone being present. Very little osteogenesis occurs as evidenced by minimal or no osteoid seam with only occasional osteoblasts. It is apparent that in the period between 8 and 12 weeks a substantial quantity of relatively mature well formed bone is present which contains osteoblasts and an osteoid seam. This appears to be an optimal time period to secure bone from a healing extraction site for grafting purposes.

Evidence suggests implants can be placed into sites with periapical and periodontal infections. The sites must be thoroughly debrided prior to placement. Guided bone regeneration is usually performed to fill the bone-implant gap and/or socket deficiencies. Although controversial, systemic antibiotics should be used until further controlled trials prove otherwise.

A relatively high incidence of infection by Actinobacillus actionomycetemcomitans can be shown in subgingival plaque samples obtained from patients with juvenile periodontitis. These organisms possess a potent leukotoxin(s) which rapidly destroys isolated human polymorphonuclear leukocytes (PMNs) and monocytes. If such leukotoxins operate in vivo, they could deprive the gingival crevice area of an essential antibacterial defense mechanism. We have found that sera from juvenile periodontitis patients consistently (greater than 90%) contain antibodies which neutralize Actinobacillus actinomycetemcomitans leukotoxin(s). On the other hand, sera from normal individuals or patients with other types of periodontal disease usually amplified rather than inhibited the leukotoxic reaction. Many patients with juvenile periodontitis have demonstrable defects in PMN or monocyte chemotaxis and this may place them at risk to gingival infection by Actinobacillus actinomycetemcomitans. The immune response against these organisms could be a crucial determinant in the course of juvenile periodontitis. While this disease is relatively rare, it does cause immeasurable emotional, physical and economic hardship for patients and their families. The identification of Actinobacillus actinomycetemcomitans as a potential pathogen in this disorder may eventually lead to specific forms of therapy to prevent and eliminate infection by this organism in these patients.

Circulating antibody levels to four strains of Actinobacillus actinomycetemcomitans (Aa) were determined by means of an indirect immunofluorescent technique in three groups of 21 subjects each, including one with juvenile periodontitis (JP), one with chronic periodontitis (CP) and one free of periodontal disease (N). Mean levels of antibody to Aa were significantly elevated in the JP group as compared to the CP and N groups with respect to strains Y4, 29522 and 29524, but not strain 29523. Since strains Y4, 29522 and 29524 contain a leukotoxin that is missing from strain 29523, the results suggest that the leukotoxin could account for the difference in the immune response among the three groups of subjects. Varying the end-point considered to represent positive fluorescence did not significantly affect the results, although discrimination among the three groups appeared to be somewhat better at lower intensities of fluorescence. Because of wide variations in antibody titers recorded in individual subjects, elevated levels of antibody to certain strains of Aa may not be useful as a primary diagnostic test for JP, but may be of value in confirming an otherwise uncertain clinical diagnosis.