The influence of controlled occlusal overload on peri-implant tissue. part 4: a histologic study in monkeys.
OBJECTIVE
The purpose of this study was to observe, after removing occlusal trauma and conducting plaque control, possible macroscopic and histologic changes in peri-implant tissue that had deteriorated resulting from experimental peri-implantitis, and to investigate the necessity for treatment procedures for peri-implantitis.


METHODS
Four monkeys (Macaca fascicularis) in good general health were used in this experiment. Three months after the second premolar and the first molar were extracted from the right mandible, 2 IMZ experimental implants were placed in each monkey. After a 3-month osseointegration period, a second surgery was conducted, followed by making an impression for fabrication of the prosthesis. Excessive occlusal height of the prosthesis was adjusted to 250 microm, and the experiment was continued for 8 weeks after placement of the prosthesis. Three models were created: (1) A superstructure with an excessive occlusal height was used for 8 weeks without any brushing (positive control, model P); (2) after the first 4 weeks with a prosthesis with excessive occlusal height and no brushing, the superstructure was removed and not used for the last 4 weeks while brushing was conducted (experimental model, model E); and (3) for 8 weeks, a prosthesis with an appropriate occlusal height was used with brushing (negative control, model N).


RESULTS
When these 3 models were compared with each other, macroscopic findings indicated inflammation only in model P. Mobility of implants was not seen in any model. Histopathologic observations revealed a slight difference between model E and model P in terms of the degree of inflammatory cell infiltration in the connective tissue.


CONCLUSIONS
No difference was found in the degree of bone resorption. Partial tearing was observed at the contact region between epithelial tissue and implant surfaces.


CONCLUSIONS
(1) The contact between implants and epithelial or connective tissue is fragile; (2) inflammation and occlusion must be controlled more prudently than in the case of natural teeth; and (3) once peri-implantitis has progressed, the control of occlusion and inflammation is probably not sufficient to promote the healing mechanism.
Miyata
Takashi
T
Department of Periodontology, School of Dentistry, Meikai University, Saitama, Japan.
Kobayashi
Yukinao
Y
Araki
Hisao
H
Ohto
Takaichi
T
Shin
Kitetsu
K
D016301:Alveolar Bone Loss / Q000209:etiology / Q000473:pathology; D000818:Animals; D001641:Bicuspid; D001732:Bite Force; D003238:Connective Tissue / Q000473:pathology; D003758:Dental Implantation, Endosseous; D015921:Dental Implants; D003769:Dental Occlusion, Traumatic / Q000150:complications* / Q000628:therapy; D003773:Dental Plaque / Q000517:prevention & control; D019094:Dental Prosthesis, Implant-Supported; D003779:Denture Design; D004848:Epithelium / Q000473:pathology; D005884:Gingival Hemorrhage / Q000209:etiology / Q000473:pathology; D008252:Macaca fascicularis; D008297:Male; D008334:Mandible / Q000601:surgery; D008963:Molar; D016348:Osseointegration; D010518:Periodontitis / Q000209:etiology / Q000473:pathology*; D010519:Periodontium / Q000473:pathology; D013314:Stress, Mechanical; D014945:Wound Healing
D015921:Dental Implants