Blockade of sympathetic b-receptors inhibits Porphyromonas gingivalis-induced alveolar bone loss in an experimental rat periodontitis model.
BACKGROUND
Periodontal disease is characterised by alveolar bone loss. Some studies have suggested the involvement of sympathetic nervous system in the deterioration of periodontal disease. Noradrenaline, released from sympathetic nerve terminals due to various stimuli, binds to specific adrenergic receptors on immune cells. Recently, we reported that restraint stress augmented the alveolar bone loss induced by Porphyromonas gingivalis infection. In this study, we investigated the effects of the beta-blocker (propranolol) on alveolar bone loss induced by P. gingivalis infection to examine the involvement of sympathetic nerves in periodontal breakdown.


METHODS
Sprague-Dawley rats were treated as follows: saline injection (Group A), propranolol injection (Group B), saline injection and oral challenge with P. gingivalis (Group C), and propranolol injection and oral challenge with P. gingivalis (Group D). Horizontal alveolar bone loss was evaluated by measuring the distance between the cemento-enamel junction and the alveolar bone crest. Specimens from periodontal tissue were evaluated by staining with hematoxylin-eosin and tartrate-resistant acid phosphatase.


RESULTS
Blockade of beta-receptors in periodontal tissue by propranolol inhibited osteoclast differentiation and prevented alveolar bone loss induced by P. gingivalis infection. Histological study revealed that the number of osteoclasts detected was proportional to the level of bone loss.


CONCLUSIONS
These results indicate that the sympathetic nervous system is involved in the development of periodontitis and suggest that sympathetic signal modulation with beta-blockers enables the control of alveolar bone mass metabolism.
Okada
Yuka
Y
Department of Craniofacial Growth and Development Dentistry, Kanagawa Dental College, Japan.
Hamada
Nobushiro
N
Kim
Yul
Y
Takahashi
Yusuke
Y
Sasaguri
Kenichi
K
Ozono
Satoru
S
Sato
Sadao
S
D000135:Acid Phosphatase / Q000032:analysis; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D016301:Alveolar Bone Loss / Q000382:microbiology / Q000517:prevention & control*; D000539:Alveolar Process / Q000187:drug effects / Q000473:pathology; D000818:Animals; D016866:Bacteroidaceae Infections / Q000382:microbiology* / Q000517:prevention & control; D015415:Biomarkers / Q000032:analysis; D001835:Body Weight; D002454:Cell Differentiation / Q000187:drug effects; D004396:Coloring Agents; D004195:Disease Models, Animal; D005456:Fluorescent Dyes; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D009929:Organ Size; D010010:Osteoclasts / Q000187:drug effects; D010518:Periodontitis / Q000382:microbiology / Q000517:prevention & control*; D016966:Porphyromonas gingivalis / Q000502:physiology*; D011433:Propranolol / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013154:Spleen / Q000473:pathology; D013564:Sympathetic Nervous System / Q000187:drug effects; D000071681:Tartrate-Resistant Acid Phosphatase; D013950:Thymus Gland / Q000473:pathology
D000319:Adrenergic beta-Antagonists; D015415:Biomarkers; D004396:Coloring Agents; D005456:Fluorescent Dyes; D007527:Isoenzymes; D011433:Propranolol; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase