title: Comparison of naturally occurring and ligature-induced peri-implantitis bone defects in humans and dogs.
abstract: OBJECTIVE
  The aim of the present study was to evaluate and compare naturally occuring and ligature-induced peri-implantitis bone defects in humans and dogs.
  
  
  METHODS
  Twenty-four partially and fully edentulous patients undergoing peri-implant bone augmentation procedures due to advanced peri-implant infections were included in this study (n=40 implants). Furthermore, peri-implantitis was induced by ligature placement and plaque accumulation in five beagle dogs for three months following implant insertion (n=15 implants). The ligatures were removed when about 30% of the initial bone was lost. During open flap surgery, configuration and defect characteristics of the peri-implant bone loss were recorded in both humans and dogs.
  
  
  RESULTS
  Open flap surgery generally revealed two different classes of peri-implant bone defects. While Class I defects featured well-defined intrabony components, Class II defects were characterized by consistent horizontal bone loss. The allocation of intrabony components of Class I defects regarding the implant body allowed a subdivision of five different configurations (Classes Ia-e). In particular, human defects were most frequently Class Ie (55.3%), followed by Ib (15.8%), Ic (13.3%), Id (10.2%), and Ia (5.4%). Similarly, bone defects in dogs were also most frequently Class Ie (86.6%), while merely two out of 15 defects were Classes Ia and Ic (6.7%, respectively).
  
  
  CONCLUSIONS
  Within the limits of the present study, it might be concluded that configurations and sizes of ligature-induced peri-implantitis bone defects in dogs seemed to resemble naturally occurring lesions in humans.
authors.affiliation: Department of Oral Surgery, Heinrich Heine University, Düsseldorf, Germany. info@frank-schwarz.de
authors.forename: Frank
authors.initials: F
authors.lastname: Schwarz
authors.forename: Monika
authors.initials: M
authors.lastname: Herten
authors.forename: Martin
authors.initials: M
authors.lastname: Sager
authors.forename: Katrin
authors.initials: K
authors.lastname: Bieling
authors.forename: Anton
authors.initials: A
authors.lastname: Sculean
authors.forename: Jürgen
authors.initials: J
authors.lastname: Becker
mesh_terms: D016301:Alveolar Bone Loss / Q000145:classification / Q000503:physiopathology; D000540:Alveolar Ridge Augmentation; D000818:Animals; D000891:Anti-Infective Agents, Local / Q000627:therapeutic use; D002710:Chlorhexidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D015921:Dental Implants / Q000009:adverse effects; D003764:Dental Materials / Q000737:chemistry; D003773:Dental Plaque / Q000150:complications; D017267:Dental Prosthesis Design; D004195:Disease Models, Animal; D004285:Dogs; D005260:Female; D006801:Humans; D007575:Jaw, Edentulous / Q000601:surgery; D007576:Jaw, Edentulous, Partially / Q000601:surgery; D008297:Male; D008875:Middle Aged; D010514:Periodontal Pocket / Q000145:classification / Q000503:physiopathology; D010518:Periodontitis / Q000145:classification / Q000503:physiopathology*; D013524:Surgical Flaps; D014025:Titanium / Q000737:chemistry; D014945:Wound Healing / Q000502:physiology
chemical_list: D000891:Anti-Infective Agents, Local; D015921:Dental Implants; D003764:Dental Materials; D014025:Titanium; C010882:chlorhexidine gluconate; D002710:Chlorhexidine