Using CBCT, occurrences of ≥2 mm maxillary facial alveolar bone were found on no more than 3% of root surfaces 1.0 to 5.0 mm apical to the bone crest in this sample of maxillary central incisors. The study evidenced prevalence of a thin facial alveolar bone (<2 mm) that may contribute to risk of facial bone fenestration, dehiscence, and soft tissue recession after immediate implant therapy.

Human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) are frequently detected in crevicular fluid of deep periodontal pockets, but little or no information is available on occurrence of herpesviruses in gingival tissue. This investigation studied the presence of herpesviruses in periodontal pockets and the corresponding gingival tissues from 11 periodontally healthy and 14 periodontitis sites. A nested-polymerase chain reaction was employed to identify the presence of HCMV, EBV-1, EBV-2, herpes simplex virus, human herpesvirus (HHV)-6, HHV-7 and HHV-8 in each test sample. In healthy periodontal sites, HCMV was detected in 1 (9%) and EBV-1 in 2 (18%) pocket samples, and HCMV was detected in 2 (18%) and EBV-1 in 3 (27%) gingival tissue samples. In periodontitis lesions, HCMV was detected in 9 (64%) pocket samples and in 12 (86%) gingival tissue samples, and EBV-1 was detected in 6 (43%) pocket samples and in 11 (79%) gingival tissue samples. HHV-6 and HHV-8 were detected exclusively in gingival tissue samples. The present findings confirm the frequent presence of HCMV and EBV-1 in periodontitis lesions and suggest using gingival tissue specimens for detecting periodontal HHV-6, HHV-7 and HHV-8.

Human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) are frequently detected in human periodontitis lesions. However, no information is available on the types of gingival cells infected by herpesviruses. The present study determined the presence of herpesviruses in polymorphonuclear neutrophils, monocytes, macrophages and T and B lymphocytes in biopsies of periodontitis lesions from 20 adults. A nested polymerase chain reaction method was employed to detect HCMV, EBV-1, EBV-2, human herpes virus-6 and herpes simplex virus (HSV) in periodontal tissue biopsy and in gingival cell fractions separated by immunomagnetic cell sorting. Tissue specimens from 18 (90%) and cell fractions from 14 (70%) patients demonstrated herpesviruses. Periodontitis-derived monocytes and macrophages revealed HCMV in cell fractions from 11 (55%) patients and HSV in cells from 1 (5%) patient. T lymphocytes harbored HCMV in cell fractions from 4 (20%) patients and HSV in cell fractions from 4 (20%) patients. B lymphocytes showed EBV-1 in cell fractions from 9 (45%) patients. Periodontal polymorphonuclear neutrophils demonstrated no herpesviruses. This study suggests that HCMV mainly infects periodontal monocytes, macrophages and less frequently T lymphocytes and that EBV-1 infects periodontal B lymphocytes. The possible etio-pathologic significance of periodontal herpesvirus infection is discussed.

The present data suggest that HCMV or EBV infections participate in the pathogenesis of periapical symptomatic lesions. Herpesviruses may produce periapical pathosis as a direct result of viral infection and replication, or as a consequence of virally induced impairment of the host defense and subsequent increased virulence of resident bacterial pathogens.

This study determined the microbial composition of the apical parts of the expanded polytetrafluoroethylene membrane surfaces facing the gingiva and the tooth in guided tissue regeneration. Microbial and clinical features of 2-to-3 wall periodontal bony defects treated with membranes with and without concomitant use of systemic Augmentin therapy were also determined. 18 patients with 18 study sites participated. 9 patients received systemic 500 mg Augmentin 1 h prior to surgery, and 500 mg TID for 8 days thereafter. 9 patients received no systemic antimicrobial therapy. Microbiological examination was performed 1 h prior to surgery, at the time of membrane removal at week 6, and at 6 months post-surgery. Microbial morphotypes, total viable counts, and the occurrence of selected microbial species were determined by phase-contrast microscopy, selective and non-selective culture, and DNA probes. Study sites were examined for probing pocket depths and attachment levels. At baseline, no microbial or clinical parameter showed statistical differences between groups. At 6 months, the Augmentin group demonstrated a significantly higher (P = 0.032; Student t-test) mean probing attachment gain (36.5% of potential gain to the cemento-enamel junction) than the 9 control patients (22.4% of potential gain). At the time of removal, membranes in the Augmentin group showed significantly fewer organisms than membranes in the control group (52.2 x 10(6) versus 488.6 x 10(6)). Sites free of pathogens on the membrane surface toward the tooth gained the most clinical attachment, even in the presence of various pathogens on the gingiva-facing membrane surface.(ABSTRACT TRUNCATED AT 250 WORDS)