Cervical sympathectomy causes alveolar bone loss in an experimental rat model.
OBJECTIVE
Periodontal disease, a pathological destructive inflammatory condition, is characterized by alveolar bone loss. Recent studies have suggested a correlation between the sympathetic nervous system and bone remodeling. To confirm the importance of the sympathetic nervous system in bone resorption, we investigated the effects of superior cervical ganglionectomy and oral challenge with Porphyromonas gingivalis on alveolar bone loss in rats.


METHODS
Rats were divided into three groups: group A underwent a sham operation as the control group; group B underwent superior cervical ganglionectomy; and group C underwent a sham operation and oral challenge with P. gingivalis. Horizontal alveolar bone loss was evaluated by measuring the distance between the cemento-enamel junction and the alveolar bone crest. Cytokine gene expression in the gingival tissues was assessed using reverse transcription-polymerase chain reaction analyses. The furcation areas of the mandibular molars were examined histologically.


RESULTS
Both superior cervical ganglionectomy and oral challenge with P. gingivalis resulted in accelerated alveolar bone loss. Gingival tissues in the superior cervical ganglionectomy group showed increased expression of the cytokines interleukin-1 alpha, tumor necrosis factor-alpha and interleukin-6. The density of neuropeptide Y-immunoreactive fibers was decreased following superior cervical ganglionectomy. Osteoclasts were observed in the superior cervical ganglionectomy and P. gingivalis-challenged groups.


CONCLUSIONS
Both superior cervical ganglionectomy and oral challenge with P. gingivalis induced alveolar bone loss. These results provide new information on the occurrence of alveolar bone loss, in that both oral challenge with P. gingivalis and superior cervical ganglionectomy are important accelerating factors for alveolar bone loss. Thus, we suggest that the sympathetic nervous system is linked with the prevention of alveolar bone loss.
Kim
Y
Y
Department of Craniofacial Growth and Development Dentistry, Division of Orthodontics, Kanagawa Dental College, Yokosuka, Japan.
Hamada
N
N
Takahashi
Y
Y
Sasaguri
K
K
Tsukinoki
K
K
Onozuka
M
M
Sato
S
S
D016301:Alveolar Bone Loss / Q000209:etiology* / Q000382:microbiology / Q000473:pathology; D000539:Alveolar Process / Q000294:innervation / Q000473:pathology; D000818:Animals; D016866:Bacteroidaceae Infections / Q000150:complications; D001835:Body Weight; D004195:Disease Models, Animal; D015171:Ganglionectomy; D005881:Gingiva / Q000276:immunology; D053582:Interleukin-1alpha / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008963:Molar / Q000473:pathology; D009478:Neuropeptide Y / Q000032:analysis; D009929:Organ Size; D010010:Osteoclasts / Q000473:pathology; D016966:Porphyromonas gingivalis / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013154:Spleen / Q000473:pathology; D017783:Superior Cervical Ganglion / Q000473:pathology / Q000601:surgery*; D013950:Thymus Gland / Q000473:pathology; D014092:Tooth Root / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D053582:Interleukin-1alpha; D015850:Interleukin-6; D009478:Neuropeptide Y; D014409:Tumor Necrosis Factor-alpha