Peri-implantitis is a destructive inflammatory process that affects the tissues around osseointegrated implants, resulting in the formation of a pen-implant pocket and loss of the supporting bony (1). Peri-implantitis are observed in 12-43% of the implants (2). The most evident clinical signs are hyperplasia of the soft tissues, suppuration, gradual bone loss and progressive mobility of the implant. One of the causes of the peri-implantitis is the bacterial colonization of implant surfaces. Lipopolysaccharides from the cell walls of periodontal pathogens induce the release by monocytes and macrophages of pro-inflammatory mediators like cytokines and tumor necrosis factor alpha. These mediators stimulate fibroblasts to produce prostaglandins and metalloproteinases, which determine the decomposition of alveolar bone and extracellular matrix destruction. In these cases, the formation of a granulation tissue can replace the bone gradually resorbed. The progression of the disease frequently leads to osteomyelitis followed by the loss of the implant after few weeks. However, the disease progression is influenced by the host response to bacterial toxins. This response depends by different factors like environmental (poor oral hygiene, smoking, stress), systemic (diabetes, osteoporosis) and genetic (polymorphisms in genes encoding molecules of the host immune defense). Microbiota associated to healthy pen-implant tissue is composed by gram-positive bacteria like Streptococcus mitis, Streptococcus sanguis and Streptococcus oralis. These microrganisms create a series of prior conditions for the adhesion of periodontal pathogens, being able to induce the development of peri-implantitis (3). The microbiota associated with failure of the implants is very similar to that found in periodontal disease and is characterized by high counts and proportions of gram-negative anaerobic bacteria. The principal microrganisms involved in penimplantitis are members of the red complex species (Poiphyromonas gingivalis, Treponema denticola and Tannerella forsythia) and orange complex species (Fusobacterium sp. and Prevotella intermedia), as defined by Socransky et al. (4). Hultin et al (5) recovered high count of A ctinobacillus actinomycetemcomitans and Aggregatibacter actinomycetemcomitans around implants with peri-implantitis. Staphylococcus aureus, enteric rods and Candida albicans, are also associated with pen-implant infections (6-8). Alcoforado et al. (9) microflora consisting Fuso bacterium species, Candida albicans. Leonhardt et al. (10) found that peri-implantitis sites are invaded by Poiphyromonas gingivalis, Porphyronionas intermedia, and Actinobacillus aclinomycetemcornitans. These pathogens were observed in ITT® and Brânemark fixtures at 3 to 6 months following implant placement (11). identified a diseased implant of Campylobacter rectus, Prevotella intermedia and fixtures at 3 to 6 months following implant placement (11)

LAB®-TEST 1: PERI-IMPLANTITIS AND BACTERIOLOGICAL ANALYSIS

GIRARDI, AMBRA;PALMIERI, ANNALISA;MARTINELLI, MARCELLA;SCAPOLI, LUCA;
2012

Abstract

Peri-implantitis is a destructive inflammatory process that affects the tissues around osseointegrated implants, resulting in the formation of a pen-implant pocket and loss of the supporting bony (1). Peri-implantitis are observed in 12-43% of the implants (2). The most evident clinical signs are hyperplasia of the soft tissues, suppuration, gradual bone loss and progressive mobility of the implant. One of the causes of the peri-implantitis is the bacterial colonization of implant surfaces. Lipopolysaccharides from the cell walls of periodontal pathogens induce the release by monocytes and macrophages of pro-inflammatory mediators like cytokines and tumor necrosis factor alpha. These mediators stimulate fibroblasts to produce prostaglandins and metalloproteinases, which determine the decomposition of alveolar bone and extracellular matrix destruction. In these cases, the formation of a granulation tissue can replace the bone gradually resorbed. The progression of the disease frequently leads to osteomyelitis followed by the loss of the implant after few weeks. However, the disease progression is influenced by the host response to bacterial toxins. This response depends by different factors like environmental (poor oral hygiene, smoking, stress), systemic (diabetes, osteoporosis) and genetic (polymorphisms in genes encoding molecules of the host immune defense). Microbiota associated to healthy pen-implant tissue is composed by gram-positive bacteria like Streptococcus mitis, Streptococcus sanguis and Streptococcus oralis. These microrganisms create a series of prior conditions for the adhesion of periodontal pathogens, being able to induce the development of peri-implantitis (3). The microbiota associated with failure of the implants is very similar to that found in periodontal disease and is characterized by high counts and proportions of gram-negative anaerobic bacteria. The principal microrganisms involved in penimplantitis are members of the red complex species (Poiphyromonas gingivalis, Treponema denticola and Tannerella forsythia) and orange complex species (Fusobacterium sp. and Prevotella intermedia), as defined by Socransky et al. (4). Hultin et al (5) recovered high count of A ctinobacillus actinomycetemcomitans and Aggregatibacter actinomycetemcomitans around implants with peri-implantitis. Staphylococcus aureus, enteric rods and Candida albicans, are also associated with pen-implant infections (6-8). Alcoforado et al. (9) microflora consisting Fuso bacterium species, Candida albicans. Leonhardt et al. (10) found that peri-implantitis sites are invaded by Poiphyromonas gingivalis, Porphyronionas intermedia, and Actinobacillus aclinomycetemcornitans. These pathogens were observed in ITT® and Brânemark fixtures at 3 to 6 months following implant placement (11). identified a diseased implant of Campylobacter rectus, Prevotella intermedia and fixtures at 3 to 6 months following implant placement (11)
2012
Carinci F ; Girardi A ; Palmieri A ; Martinelli M ; Scapoli L ; Avantaggiato A; Nardi GM ; Lauritano D
File in questo prodotto:
Eventuali allegati, non sono esposti

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/499974
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 52
  • ???jsp.display-item.citation.isi??? 27
social impact