Three-dimensional changes of a porcine collagen matrix and free gingival grafts for soft tissue augmentation to increase the width of keratinized tissue around dental implants: a randomized controlled clinical study.

BACKGROUND: Emerging clinical data points to the relevance of the presence of keratinized tissue (KT). Although apically positioned flap/vestibuloplasty along with free gingival graft (FGG) is considered as a standard intervention for augmenting KT, substitute materials appear to be a viable treatment alternative. So far, there is a lack of data investigating the dimensional changes at implant sites treated with soft-tissue substitutes or FGG. AIM: The present study aimed at comparing three-dimensional changes of a porcine derived collagen matrix (CM) and FGG for increasing KT at dental implants over a 6-month follow-up period. MATERIALS AND METHODS: The study enrolled 32 patients exhibiting deficient KT width (i.e., < 2 mm) at the vestibular aspect who underwent soft tissue augmentation using either CM (15 patients/23 implants) or FGG (17 patients/31 implants). The primary outcome was defined as tissue thickness change (mm) at treated implant sites between 1- (S0), 3- (S1), and 6-months (S2). Secondary outcomes considered changes of KT width over a 6-month follow-up period, surgical treatment time, and patient-reported outcomes. RESULTS: Dimensional analyses from S0 to S1 and from S0 to S2 revealed a mean decrease in tissue thickness of - 0.14 ± 0.27 mm and - 0.04 ± 0.40 mm in the CM group, and - 0.08 ± 0.29 mm and - 0.13 ± 0.23 mm in the FGG group, with no significant differences noted between the groups (3 months: p = 0.542, 6 months: p = 0.659). Likewise, a comparable tissue thickness decrease was observed from S1 to S2 in both groups (CM: - 0.03 ± 0.22 mm, FGG: - 0.06 ± 0.14 mm; p = 0.467). The FGG group exhibited a significantly greater KT gain after 1, 3 and 6 months compared to the CM group (1 month: CM: 3.66 ± 1.67 mm, FGG: 5.90 ± 1.58 mm; p = 0.002; 3 months: CM: 2.22 ± 1.44; FGG: 4.91 ± 1.55; p = 0.0457; 6 months: CM: 1.45 ± 1.13 mm, FGG: 4.52 ± 1.40 mm; p < 0.1). Surgery time (CM: 23.33 ± 7.04 min.; FGG: 39.25 ± 10.64 min.; p = 0.001) and postoperative intake of analgesics were significantly lower in the CM group (CM: 1.2 ± 1.08 tablets; FGG: 5.64 ± 6.39 tablets; p = 0.001). CONCLUSIONS: CM and FGG were associated with comparable three-dimensional thickness changes between 1 and 6 months. While a wider KT band could be established with FGG, the use of CM significantly reduced surgical time and patients´ intake of analgesics.

Glucosamine inhibits extracellular matrix accumulation in experimental diabetic nephropathy.

Introduction: Glucosamine, the intermediate metabolite of the hexosamine biosynthesis pathway (HBP), is widely used as a supplementary drug in patients with osteoarthritis. However, its consequences in such patients concomitantly suffering from diabetic nephropathy is unknown. Methods: The aim of the study was to investigate the effect of exogenous administration of glucosamine in the diabetic kidney. A mouse model of streptozotocin-induced diabetic nephropathy in vivo and cultured endothelial cells in vitro were used in the study. The mice were treated with glucosamine for 6 months. Renal function was evaluated by metabolic cage, and histology of the kidney was estimated by periodic acid-schiff (PAS) staining. The expression of related genes was assessed by real-time PCR, immunofluorescence staining, immunoblotting and ELISA. Results: There was no significant difference in urinary albumin secretion, relative kidney weight, or creatinine clearance between the groups treated with glucosamine and controls. Assessment of the kidney demonstrated reduction in mesangial expansion and fibronectin expression in the diabetic glomeruli treated with glucosamine. Glucosamine treatment significantly decreased α-smooth muscle actin (α-SMA) protein expression in both diabetic and control kidneys, whereas the expression of other fibrosis-related genes and inflammatory factors was unaltered. Moreover, α-SMA colocalized with the endothelial marker CD31 in the diabetic and control kidneys, and glucosamine reduced α-SMA+ ECs in the diabetic glomeruli. In addition, glucosamine suppressed α-SMA expression in endothelial cells treated with or without high glucose. Discussion: In summary, this is the first report to show that glucosamine reduces mesangial expansion and inhibits endothelial-mesenchymal transition in diabetic nephropathy. The underlying mechanisms need to be further investigated.