Effects of mechanical stimulation by a powered toothbrush on the healing of periodontal tissue in a rat model of periodontal disease.
OBJECTIVE
Elimination of pathogens is the main aim of periodontal treatment; however, modulation of the host immune response should also be considered. This study aimed to evaluate the effects of mechanical stimulation on periodontal healing in rats.


METHODS
Before starting the experiment, lipopolysaccharide and proteases were applied once a day, for 4 wk, to both maxillary first molars of 30 rats to induce periodontal disease, and the application was stopped at the end of the 4-wk period. The experiment started immediately following this pretreatment. In the experiment, the left palatal gingiva was stimulated once daily using a powered toothbrush and the right gingiva served as a control (no mechanical stimulation). Pathological changes, and proliferation and cell death in periodontal tissues, were evaluated histometrically and immunohistochemically at baseline (0 wk), and at 1 and 3 wk of stimulation.


RESULTS
The control showed a reduction of polymorphonuclear leukocyte infiltration in connective tissue and an increase in the numbers of gingival and periodontal ligament fibroblasts. Mechanical stimulation reduced polymorphonuclear leukocyte infiltration and the area of destroyed collagen in connective tissue, and increased the number of gingival fibroblasts; however, it had no effect on alveolar bone and root resorption or on the number of periodontal ligament fibroblasts.


CONCLUSIONS
Mechanical stimulation accelerated the healing of gingival inflammation by reducing the infiltration of polymorphonuclear leukocytes and enhancing fibroblast proliferation and collagen synthesis.
Ekuni
D
D
Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Yamanaka
R
R
Yamamoto
T
T
Miyauchi
M
M
Takata
T
T
Watanabe
T
T
D016301:Alveolar Bone Loss / Q000473:pathology / Q000503:physiopathology; D000539:Alveolar Process / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D001426:Bacterial Proteins / Q000009:adverse effects; D016923:Cell Death / Q000502:physiology; D049109:Cell Proliferation; D003094:Collagen; D003238:Connective Tissue / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D004846:Epithelial Attachment / Q000473:pathology / Q000503:physiopathology; D004926:Escherichia coli; D005347:Fibroblasts / Q000473:pathology; D005881:Gingiva / Q000473:pathology / Q000503:physiopathology; D005891:Gingivitis / Q000473:pathology / Q000503:physiopathology; D008070:Lipopolysaccharides / Q000009:adverse effects; D008297:Male; D020556:Neutrophil Infiltration / Q000502:physiology; D009504:Neutrophils / Q000473:pathology; D010447:Peptide Hydrolases / Q000009:adverse effects; D010510:Periodontal Diseases / Q000473:pathology / Q000503:physiopathology*; D010513:Periodontal Ligament / Q000473:pathology / Q000503:physiopathology; D010812:Physical Stimulation; D051381:Rats; D017208:Rats, Wistar; D012391:Root Resorption / Q000473:pathology / Q000503:physiopathology; D013305:Streptomyces griseus; D013997:Time Factors; D014099:Toothbrushing / Q000295:instrumentation*; D014945:Wound Healing / Q000502:physiology
D001426:Bacterial Proteins; D008070:Lipopolysaccharides; D003094:Collagen; D010447:Peptide Hydrolases