GBRs are essential procedures in implant dentistry and periodontology where barrier membranes play an important role by isolating soft tissue and allowing bone to grow. Not all membranes function the same way, as they differ from their origin and structure, it is important to understand how membranes behave and differ one from others in order to achieve a predictable treatment. A systematic search on Medline by two independent reviewers was performed for articles published until July 2017 reporting the characteristics or properties of barrier membranes. The question that preceded the search was designed according to PICO rules. A total of 124 articles were initially identified from electronic searching. After abstract/full-text review, 21 were included for a systematic review. According to the extracted data and article analysis, barrier membranes should fulfill the following criteria in order to success: biocompatibility, space maintaining, occlusive function, easy - handling and a bioactivation friendly property. With the development of new biomaterials and surfaces, a great advance in this area is expected. It has been clearly described that biocompatibility is the most important requirement to take into account when choosing a membrane, but other factors such as space maintaining capacity, cell oclusiveness, easy handling and bioactivation friendly materials are the ones that will fulfill our necessities. Key words:Barrier membrane, guided bone regeneration, dental implantology, oral surgery, collagen membrane, biomaterial.

A short inflammatory phase and fast ingrowth of blood vessels and mesenchymal cells are essential for tissue integration of a biomaterial. Macrophages play a key role in this process. We investigated invasion of macrophages, blood vessels, and proliferating cells into a highly porous and volume-stable collagen matrix (VCMX) used for soft tissue augmentation around teeth and dental implants. The biomaterial was implanted in submucosal pouches in the canine maxilla, and the tissue response was analyzed at six different time points. Immunohistochemistry was done for proliferating cells (PCNA), macrophages (MAC387), multinucleated giant cells (CD86), and blood vessels (TGM2). Blood rapidly filled the VCMX pores. During the first week, MAC387+ cells populated the VCMX pores, blood vessels and PCNA+ cells invaded the VCMX, and CD86+ scattered cells were observed. At 15 days, MAC387+ cells were scanty, blood vessels had completely invaded the VCMX, the number of proliferating cells peaked, and fibroblasts appeared. At 30 days, MAC387+ were absent, the numbers of proliferating and CD86+ cells had declined, while blood vessel and fibroblast numbers were high. At 90 days, residual VCMX was well-integrated in soft connective tissue. In conclusion, the VCMX elicited a short inflammatory phase followed by rapid tissue integration.

Collagen-based scaffolds hold great potential for tissue engineering, since they closely mimic the extracellular matrix. We investigated tissue integration of an engineered porous collagen-elastin scaffold developed for soft tissue augmentation. After implantation in maxillary submucosal pouches in 6 canines, cell invasion (vimentin), extracellular matrix deposition (collagen type I) and scaffold degradation (cathepsin k, tartrate-resistant acid phosphatase (TRAP), CD86) were (immuno)-histochemically evaluated. Invasion of vimentin⁺ cells (scattered and blood vessels) and collagen type I deposition within the pores started at 7 days. At 15 and 30 days, vimentin⁺ cells were still numerous and collagen type I increasingly filled the pores. Scaffold degradation was characterized by collagen loss mainly occurring around 15 days, a time point when medium-sized multinucleated cells peaked at the scaffold margin with simultaneous labeling for cathepsin k, TRAP, and CD86. Elastin was more resistant to degradation and persisted up to 90 days in form of packages well-integrated in the newly formed soft connective tissue. In conclusion, this collagen-based scaffold maintained long-enough volume stability to allow an influx of blood vessels and vimentin⁺ fibroblasts producing collagen type I, that filled the scaffold pores before major biomaterial degradation and collapse occurred. Cathepsin k, TRAP and CD86 appear to be involved in scaffold degradation.