Recession coverage using the modified coronally advanced tunnel and connective tissue graft with or without enamel matrix derivative: 5-year results of a randomised clinical trial.

OBJECTIVES: To evaluate the 5-year results of single and multiple recession type (RT) 1 and 2 (Miller I to III) recessions treated with the modified coronally advanced tunnel (MCAT) and connective tissue graft (CTG) with or without an enamel matrix derivative (EMD). The main outcome variable was the stability of obtained root coverage from 6 months to 5 years. MATERIALS AND METHODS: In 24 patients, both complete and mean root coverage (CRC and MRC) and gain of keratinised tissue (KT) were assessed at 6 months and 5 years after recession coverage by means of MCAT and CTG with or without EMD. Aesthetic outcomes after 5 years were evaluated using the root coverage aesthetic score (RES). RESULTS: At 5 years, 24 patients with a total of 43 recessions were evaluated. Eight patients (57.14%) of the test and 6 (60.0%) of the control group showed complete root coverage. MRC revealed no statistically significant differences between the two groups, with 73.87 ± 26.83% (test) and 75.04 ± 22.06% (control), respectively. KT increased from 1.14 ± 0.57 mm to 3.07 ± 2.27 mm in the test group and from 1.24 ± 0.92 mm to 3.02 ± 1.55 mm in the control group, respectively. CONCLUSION: Treatment of single and multiple RT 1 and 2 recessions by means of MCAT and CTG with or without EMD yielded comparable clinical improvements which could be maintained over a period of 5 years. The additional use of EMD did not influence the clinical outcomes. CLINICAL RELEVANCE: The use of MCAT + CTG yielded successful coverage of single and multiple RT 1 and 2 gingival recessions, while the additional application of EMD did not seem to influence the results.

Treatment of multiple adjacent RT 1 gingival recessions with the modified coronally advanced tunnel (MCAT) technique and a collagen matrix or palatal connective tissue graft: 9-year results of a split-mouth randomized clinical trial.

OBJECTIVES: To evaluate t he long-term outcomes following treatment of RT 1 multiple adjacent gingival recessions (MAGR) using the modified coronally advanced tunnel (MCAT) with either a collagen matrix CM or a connective tissue graft (CTG). MATERIAL AND METHODS: Sixteen of the original 22 subjects included in a randomized, controlled split-mouth clinical trial were available for the 9-year follow-up (114 sites). Recessions were randomly treated by means of MCAT + CM (test) or MCAT + CTG (control). Complete root coverage (CRC), mean root coverage (MRC), gingival recession depth (GRD), probing pocket depth (PD), keratinized tissue width (KTW), and thickness (KGT) were compared with baseline values and with the 12-month results. RESULTS: After 9 years, CRC was observed in 2 patients, one in each group. At 9 years, MRC was 23.0 ± 44.5% in the test and 39.7 ± 35.1% in the control group (p = 0.179). The MRC reduction compared to 12 months was - 50.1 ± 47.0% and - 48.3 ± 37.7%, respectively. The upper jaw obtained 31.92 ± 43.0% of MRC for the test and 51.1 ± 27.8% for the control group (p = 0.111) compared to the lower jaw with 8.3 ± 46.9% and 20.7 ± 40.3%. KTW and KGT increased for both CM and CTG together from 2.0 ± 0.7 to 3.1 ± 1.0 mm (< 0.0001). There were no statistically significant changes in PD. CONCLUSION: The present results indicate that (a) treatment of MAGR using MCAT in conjunction with either CM or CTG is likely to show a relapse over a period of 9 years, and (b) the outcomes obtained in maxillary areas seem to be more stable compared to the mandibular ones. CLINICAL RELEVANCE: The mean root coverage at 12 months could not be fully maintained over 9 years. On a long-term basis, the results seem to be less stable in the mandible as compared to maxillary areas.

Common target genes of palatal and gingival fibroblasts for EMD: the microarray approach.

BACKGROUND AND OBJECTIVE: Connective tissue grafts are frequently applied, together with Emdogain(®) , for root coverage. However, it is unknown whether fibroblasts from the gingiva and from the palate respond similarly to Emdogain. The aim of this study was therefore to evaluate the effect of Emdogain(®) on fibroblasts from palatal and gingival connective tissue using a genome-wide microarray approach. MATERIAL AND METHODS: Human palatal and gingival fibroblasts were exposed to Emdogain(®) and RNA was subjected to microarray analysis followed by gene ontology screening with Database for Annotation, Visualization and Integrated Discovery functional annotation clustering, Kyoto Encyclopedia of Genes and Genomes pathway analysis and the Search Tool for the Retrieval of Interacting Genes/Proteins functional protein association network. Microarray results were confirmed by quantitative RT-PCR analysis. RESULTS: The transcription levels of 106 genes were up-/down-regulated by at least five-fold in both gingival and palatal fibroblasts upon exposure to Emdogain(®) . Gene ontology screening assigned the respective genes into 118 biological processes, six cellular components, eight molecular functions and five pathways. Among the striking patterns observed were the changing expression of ligands targeting the transforming growth factor-beta and gp130 receptor family as well as the transition of mesenchymal epithelial cells. Moreover, Emdogain(®) caused changes in expression of receptors for chemokines, lipids and hormones, and for transcription factors such as SMAD3, peroxisome proliferator-activated receptor gamma and those of the ETS family. CONCLUSION: The present data suggest that Emdogain(®) causes substantial alterations in gene expression, with similar patterns observed in palatal and gingival fibroblasts.

Surgical suturing of articular cartilage induces osteoarthritis-like changes.

INTRODUCTION: In clinical tissue-engineering-based approaches to articular cartilage repair, various types of flap are frequently used to retain an implanted construct within the defect, and they are usually affixed by suturing. We hypothesize that the suturing of articular cartilage is associated with a loss of chondrocytes from, and osteoarthritis-like changes within, the perisutural area. MATERIALS AND METHODS: We established a large, partial-thickness defect model in the femoral groove of adult goats. The defects were filled with bovine fibrinogen to support a devitalized flap of autologous synovial tissue, which was sutured to the surrounding articular cartilage with single, interrupted stitches. The perisutural and control regions were analyzed histologically, histochemically and histomorphometrically shortly after surgery and 3 weeks later. RESULTS: Compared to control regions, chondrocytes were lost from the perisutural area even during the first few hours of surgery. During the ensuing 3 weeks, the numerical density of cells in the perisutural area decreased significantly. The cell losses were associated with a loss of proteoglycans from the extracellular matrix. Shortly after surgery, fissures were observed within the walls of the suture channels. By the third week, their surface density had increased significantly and they were filled with avascular mesenchymal tissue. CONCLUSIONS: The suturing of articular cartilage induces severe local damage, which is progressive and reminiscent of that associated with the early stages of osteoarthritis. This damage could be most readily circumvented by adopting an alternative mode of flap affixation, such as gluing with a biological adhesive.