Periimplantitis

2. Aetiology and epidemiology

Mucositis and peri-implantitis occur with a prevalence of about 63.4% and 5% to 47.1% respectively, with the large fluctuations attributable to different study designs and population sizes in the publications with varying risk profiles and calculation profiles (SCHWARZ et al., 2008, ATIEH et al., 2012; CHARYEVA et al., 2012; SCHLOTTIG, 2011; ZITZMANN & BERGLUNDH, 2008, Smeets et al., 2014a).

ZITZMANN & BERGLUNDH (2008) quantified the incidence of the development of peri-implantitis in patients with prior periodontitis as being almost six times higher than for patients with no previous history of periodontal inflammatory formations.

After 10 years, between 10% and 50% of all implants showed signs of peri-implantitis (ROOS-JANSÅKER et al., 2007; BEHRENS et al., 2004). According to the consensus report of the sixth European Workshop on Periodontology, LINDHE & MEYLE (2008) reported the frequency of mucositis as being 80% and that of peri-implantitis as 28% to 56% among patients with implant restorations. The prevalence of peri-implantitis was corrected by MOMBELLI et al. (2012) to 20% of all implant patients and 10% of all implants. The correction downwards was explained by the fact that to correctly determine the prevalence, only those studies can be considered in which the bone loss relevant for the peri-implantitis was determined from the time the suprastructure was inserted (baseline). This led to the recommendation for carrying out radiographic imaging after inserting the suprastructure and using this as the foundation for future evaluation of any peri-implant bone losses. Spectra consisting of P. intermedia/nigrescens, S. constellatus, A. actinomycetemcomitans, P. gingivalis, T. denticola und T. forsythia among others have been verified as marker bacteria.

Excursus 1 Marker bacteria in the subgingival biofilm
Complex Marker bacterium Characteristics
Actinobacillus
actinomycetemcomitans
  • Complex-independent
  • Signi cant at almost every level
  • Toxin-ProduzentProduces toxin
  • Invasive
A Porphyromonas
gingivalis
  • Obligate anaerobe
  • Primary periodontal pathogen
  • Has a great number of proteases
  • Heavily involved in collagen and antibody degradation
Tannerella
forsythensis
  • Obligate anaerobe
  • Very important for the clinical progression of periodontitis
  • High level of protease activity
  • Produces volatile fatty acids
Treponema
denticola
  • Obligate anaerobe
  • Periodontal pathogen
  • Degrades proteins
  • Produces volatile fatty acids
B Campylobacter
gracilis
  • Microaerophile
  • Importance in periodontal processes speculative
Campylobacter
rectus
  • Microaerophile
  • Is often isolated with periodontitis
  • Produces a cytotoxin (similar to leukotoxin; A. actinomycetemcomitans)
Eubacterium
nodatum
  • Obligate anaerobe
  • Gram-positive
  • Potential periodontal pathogen
  • Cell count is elevated in periodontal processes
Fusobacterium
nucleatum
  • Obligate anaerobe
  • Early coloniser
Peptostreptococus
micros
  • Obligate anaerobe
  • Relatively well established Gram-positive periodontal pathogen
  • Also present physiologically
  • Protein breakdown
  • Early marker
B Prevotella
intermedia
  • Obligate anaerobe
  • Early marker bacterium
  • Creates the anaerobic environment for the primary pathogens by consuming oxygen
  • Easy and widespread colonisation of mucous membranes
Prevotella
nigrescens
  • Obligate anaerobe
  • Important role in infections of the tooth root
  • Similar properties to P. intermedia
  • Role is hotly disputed
  • Besiedelt gerne und zahlreich Schleimhäute
C Streptococcus
gordonii
  • Facultative anaerobe
  • Early coloniser
  • Considered physiological if isolated
Streptococcus
mitis
  • Facultative anaerobe
  • Considered physiological if isolated
D Campylobacter
concisius
  • Microaerophile
  • Speculative importance
Capnocytophaga
gingivalis
  • Of importance in periodontal diseases that develop early (prepuberty)
Eikenella
corrodens
  • Aerobe or facultative anaerobe
  • Cell count is elevated in periodontal processes
E Actinomyces
odontolyticus
  • Physiological marker
  • Anaerobe to microaerophile
  • According to Socransky (1998), forms a complex with Veillonella parvula that is of minimal importance for periodontitis
Actinomyces
viscosus
  • Physiological marker
  • Anaerobe to microaerophile
Veillonella
parvula
  • Obligate anaerobe
  • Gram-negative
  • Minimal periodontal pathogenic importance
  • Catabolises lactic acid
  • Possibly anti-cariogenic
  • Increases the mineralisation of dental plaque to form calculus

Bacteria in complex A are associated strongly with deep pockets and bleeding on probing (BOP), while bacteria in complex B have a significantly increased association with the pocket depth. The bacterial communities in complexes C, D and E can be classified as physiological in isolation and when diagnosed as a collective are possibly of importance in processes in periodontitis and peri-implantitis. Modified from Socransky (1998).

Depending on the type and antibiotic, variable levels of resistance of the individual pathogens have been described (Tab. 2) (ZITZMANN & BERGLUNDH, 2008; RAMS et al., 2014). According to RAMS et al. (2014), of 120 patients a total of 71.7% displayed resistance against at least one active substance.

Table 2: Antibiotic resistance
Antibiotic Resistance
Clindamycin 46,7 %
Amoxicillin 39,2 %
Doxycyclin 25,0 %
Metronidazol 21,7 %
Amoxicilin & Metronidazol 6,7 %

Antibiotic resistance in Prevotella intermedia/nigrescens and Steptococcus constellatus (n=120) (RAMS et al., 2014)

A fundamental difference to periodontitis is that, in addition to the known marker periodontal bacteria, Staphylococcus aureus in particular appears to play an important role in peri-implantitis. This bacterium has a high affinity for titanium and has a high positive (80%) and a high negative (90%) predictive value according to studies carried out by SALVI et al. (2008).

The occurrence of peri-implantitis can be influenced by the surface properties of the implant shoulder. However, current data cannot conclusively confirm whether a rough or a smooth surface favours the development of peri-implantitis (DEGIDI et al., 2012, SCHLOTTIG, 2011, SUBRAMANI et al., 2009).