Original study - ZZI 01/2011

Comparative microarray analyses of inflamed human periimplant and periodontal tissues in vivo

F. vom Orde1, M. Rödiger2, N. Gersdorff2

Purpose: The aim of the present in vivo study was a comparative gene expression analysis of inflamed periimplant and periodontal tissues to demonstrate potential differences between these two disease entities at the molecular level. The data presented here was combined from two published studies [7, 17].

Materials and methods: Using microarray technology, the gene expression profiles of inflamed periimplant tissue, inflamed and healthy periodontal tissue were analyzed and verified by real-time (RT) PCR. The main focus was on extracellular matrix components as well as on their degrading enzymes.

Results: In inflamed periimplant tissue, non-fibril-forming collagens types IV, VI, VII and XVII were up-regulated and the fibril-forming type III and XI collagens were down-regulated compared to inflamed periodontal tissue. In the group of matrix-degrading enzymes, the cathepsins B and C, the matrix metalloproteinases MMP-1 and MMP-9 were up-regulated and two tissue inhibitors of metalloproteinases, TIMP-1 and TIMP-3, were significantly up-regulated.

Conclusions: In summary, the results of the present study show that periimplantitis can be clearly differentiated from periodontitis at the molecular level. Comparison of these two oral diseases might be important for the objectification of disease-specific genes, and for the diagnosis, progress and prognosis as well as for the development of new periimplantitis therapies.

Keywords: periimplantitis; periodontitis; microarray; real-time (RT) PCR; extracellular matrix


Oral implantology has achieved a significant position in modern dentistry. The long-term clinical prognosis of dental implants depends on their adequate integration into the surrounding tissues (epithelium, connective tissue and bone).

Similar demands are made of periimplant tissue as of periodontal tissue: support and anchoring functions, tissue adaptability towards functional irritants and protection against harmful substances in the mouth. In contrast to the teeth, which develop together with their supporting tissues, endosteal implants are inserted in a surgically prepared recipient site (Fig. 1). In consequence, the periimplant tissues are the result of a wound healing process. Unlike the gingiva, the periimplant anatomical structures exhibit scar tissue with weakened defenses [3]. Despite this weakened resistance, dental implants demonstrate outstanding long-term results. Nevertheless, in spite of the best efforts, biological and technical failures before and during the prosthetic functional loading period cannot be avoided in every case [15]. In recent years, it has become apparent that biological failures in particular, especially periimplant infections (periimplantitis), are a significant problem [2]. These are characterized especially by the formation of gingival pockets with inflammation around the implant neck, associated with progressive loss of soft tissue and alveolar bone, possibly culminating in implant loosening or loss.

The European Federation of Periodontology for the first time defined periimplantitis clearly in 1993 as follows: if the pathological changes of osseointegrated implants are limited to the soft tissue, this is called periimplant mucositis; if inflammatory bone atrophy is found as well as soft tissue inflammation, this is known as periimplantitis. However, in contrast to periodontitis, periimplantitis is always a local osteitis, as the protective and highly immunocompetent periodontium is absent in the case of implants [10].

The problem of periimplantitis has become more and more important in recent years. This is due especially to the fact that cases of periimplant infection have increased as the number of implantations increased [15, 19]. In addition, it is known that the likelihood of failed implantation increases by 30 % if implant loss occurred previously [24]. A further problem is that when periimplantitis is present, treatment is time-consuming and expensive and success is very uncertain.

The extracellular matrix (ECM)

ECM is the part of the tissue that is secreted by cells into the intercellular space. On a superficial level, the function of the ECM is to fix the cells embedded in it. However, if the ECM is considered precisely, it is found that the ECM interacts with the cells lying within it. The components of the ECM are synthesized and secreted by cells but are degraded extracellularly or intracellularly (after endocytosis). Moreover, expression of genes in the cells is regulated by binding of cell receptors to certain components of the ECM.

The ECM consists for the most part of different proteins and glycoproteins along with polysaccharides. The ECM can be subdivided into the collagen family, glycosaminoglycans and non-collagen glycoproteins.

The collagen family currently includes 27 different collagens (collagen I – collagen XXVII), which constitute most of the protein content of the ECM [11]. The great variety of collagen types and the arrangement and cross-linking of the collagen fibrils form an important basis for the mechanical stability of the tissue. Apart from fibril-forming collagens such as collagen type I, II and III, non-fibril-forming collagens can be distinguished. Collagen type IV is an example of a non-fibril-forming collagen; this forms a three-dimensional mesh and so is one of the most important components of basement membranes.

All collagens are synthesized by a number of cells (fibro-blasts, chondroblasts and osteoblasts) and secreted into the ECM. In the periodontium the collagen fibers (Sharpey fibers) have the task of anchoring the tooth in the bony socket.

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