Modulation of clinical expression of plaque-induced gingivitis. I. Background review and rationale.

OBJECTIVES: The purpose of this article is to provide the necessary background and rationale for the accompanying studies, which are ultimately aimed at identifying genetic and environmental factors determining gingivitis susceptibility. MATERIALS AND METHODS: The literature on factors reported to modify the clinical expression of gingivitis, i.e., factors that determine individual variability in gingival inflammatory response to plaque, is presented. RESULTS: Clinical evidence suggests that the gingival inflammatory response to plaque accumulation may differ substantially among individuals. However, most of the available studies are of small scale and not purposely designed to address the issue. Systemic factors implicated in modulation of the clinical expression of gingivitis include metabolic, genetic, environmental and other factors. The significance of such factors in designing and conducting a large-scale experimental gingivitis trial and means to account for them are discussed. CONCLUSION: Although several factors have been implicated, genetic or environmental factors underlying differences in gingivitis expression are not fully elucidated. The accompanying studies aim to identify and characterize, among participants in a specifically designed large-scale experimental gingivitis trial, subjects that differ significantly in their gingival inflammatory response to plaque. This is the first step in an effort to determine genetic or environmental factors underlying such differences

Adverse effects associated with the use of an absorbable GTR device in the treatment of human gingival recession defects. A clinicopathologic case report.

This clinicopathologic case report documents an adverse effect associated with the use of a polylactic acid-based barrier in the treatment of human gingival recession defects. A total of 27 consecutively treated patients, in whom guided tissue regeneration with a polylactic acid barrier was used to correct gingival recession defects, were evaluated. This adverse effect consisted of a midradicular-apical swelling, generally asymptomatic, with no apparent predilection for gender, age, tooth type or location (maxilla/mandible), or surgical procedure. It was observed in 14 of 27 (52%) patients and 22 of 41 (54%) defects. The swelling decreased in size over time and in most cases, it completely resolved within 12 months postsurgery. Histopathologic evaluation of a 14-week specimen indicated characteristics (multinucleated giant cells, foamy macrophages) consistent with a foreign body reaction. These findings suggest that patients undergoing GTR procedures with synthetic absorbable devices for the treatment of gingival recession defects should be advised of the possible occurrence of such an adverse effect

Gingival Perfusion and Tissue Biomarkers During Early Healing of Postextraction Regenerative Procedures: A Prospective Case Series

Background—Post-extraction alveolar bone loss, mostly affecting the buccal plate, occurs despite regenerative procedures. To better understand possible determinants, this prospective case series assessed gingival blood perfusion and tissue molecular responses in relation to postextraction regenerative outcomes. Methods—Adults scheduled to receive bone grafting in maxillary, non-molar, single tooth extraction site were recruited. Clinical documentation included probing pocket depth (PD), keratinized tissue width (KT), tissue biotype (TB), plaque (P) and bleeding. Wound closure was clinically evaluated. Gingival blood perfusion was measured by Laser Doppler Flowmetry (LDF). Wound fluid (WF) and gingival biopsies were analyzed for protein levels and gene expression, respectively, of relevant molecular markers. Bone healing outcomes were determined radiographically (Cone Beam Computerized Tomography; CBCT). Healing was followed for 4 months. Results—Data from 15 patients (50 ± 5 years, 8 males) are reported. Postoperatively, neither complications nor changes in PD, KT or TB were observed. Postoperatively, LDF revealed decreased perfusion followed by hyperemia that persisted 1 month (p≤0.05). WF levels of angiopoietin-2, interleukin-8, tumor necrosis factor-α, and vascular endothelial growth factor peaked on day 6 (p≤0.05) and decreased thereafter. Only interleukin-8 and tumor necrosis factor-α exhibited increased gene expression. Linear bone changes were negligible. Volumetric bone changes were minimal but statistically significant, with more bone loss when membrane was used (p=0.05). Conclusion—Gingival blood perfusion following post-extraction bone regenerative procedures follows an ischemia-reperfusion model. Transient increases in angiogenic factor levels and prolonged hyperemia characterize the soft tissue response. These soft tissue responses do not determine radiographic bone changes

Bone Grafting History Affects Soft Tissue Healing Following Implant Placement

Background This study aimed to determine and compare soft tissue healing outcomes following implant placement in grafted (GG) and non-grafted bone (NGG). Methods Patients receiving single implant in a tooth-bound maxillary non-molar site were recruited. Clinical healing was documented. Volume and content of wound fluid (WF; at 3, 6, and 9 days) were compared with adjacent gingival crevicular fluid (GCF; at baseline, 1, and 4 months). Buccal flap blood perfusion recovery and changes in bone thickness were recorded. Linear mixed model regression analysis and generalized estimating equations with Bonferroni adjustments were conducted for repeated measures. Results Twenty-five patients (49 ± 4 years; 13 males; nine NGG) completed the study. Soft tissue closure was slower in GG (P \u3c 0.01). Differential response in WF/GCF protein concentrations was detected for ACTH (increased in GG only) and insulin, leptin, osteocalcin (decreased in NGG only) at day 6 (P ≤0.04), with no inter-group differences at any time(P \u3e 0.05). Blood perfusion rate decreased immediately postoperatively (P \u3c 0.01, GG) followed by 3-day hyperemia (P \u3e 0.05 both groups). The recovery to baseline values was almost complete for NGG whereas GG stayed ischemic even at 4 months (P = 0.05). Buccal bone thickness changes were significant in GG sites (P ≤ 0.05). Conclusion History of bone grafting alters the clinical, physiological, and molecular healing response of overlying soft tissues after implant placement surgery

Loss of discoidin domain receptor 1 predisposes mice to periodontal breakdown

The discoidin domain receptors, DDR1 and DDR2, are nonintegrin collagen receptors and tyrosine kinases. DDRs regulate cell functions, and their extracellular domains affect collagen fibrillogenesis and mineralization. Based on the collagenous nature of dentoalveolar tissues, we hypothesized that DDR1 plays an important role in dentoalveolar development and function. Radiography, micro-computed tomography (micro-CT), histology, histomorphometry, in situ hybridization (ISH), immunohistochemistry (IHC), and transmission electron microscopy (TEM) were used to analyze Ddr1 knockout (Ddr1(-/-)) mice and wild-type (WT) controls at 1, 2, and 9 mo, and ISH and quantitative polymerase chain reaction (qPCR) were employed to assess Ddr1/DDR1 messenger RNA expression in mouse and human tissues. Radiographic images showed normal molars but abnormal mandibular condyles, as well as alveolar bone loss in Ddr1(-/-) mice versus WT controls at 9 mo. Histological, histomorphometric, micro-CT, and TEM analyses indicated no differences in enamel or dentin Ddr1(-/-) versus WT molars. Total volumes (TVs) and bone volumes (BVs) of subchondral and ramus bone of Ddr1(-/-) versus WT condyles were increased and bone volume fraction (BV/TV) was reduced at 1 and 9 mo. There were no differences in alveolar bone volume at 1 mo, but at 9 mo, severe periodontal defects and significant alveolar bone loss (14%; P < 0.0001) were evident in Ddr1(-/-) versus WT mandibles. Histology, ISH, and IHC revealed disrupted junctional epithelium, connective tissue destruction, bacterial invasion, increased neutrophil infiltration, upregulation of cytokines including macrophage colony-stimulating factor, and 3-fold increased osteoclast numbers (P < 0.05) in Ddr1(-/-) versus WT periodontia at 9 mo. In normal mouse tissues, ISH and qPCR revealed Ddr1 expression in basal cell layers of the oral epithelia and in immune cells. We confirmed a similar expression pattern in human oral epithelium by ISH and qPCR. We propose that DDR1 plays an important role in periodontal homeostasis and that absence of DDR1 predisposes mice to periodontal breakdown98131521153