The effect of interleukin-11 on the progression of ligature-induced periodontal disease in the beagle dog.
BACKGROUND
The rate of progression of periodontal disease is dependent on the complex regulatory interactions between bacteria and the immune modulators of the host response. The purpose of this investigation was to determine if recombinant human interleukin-11 (rhIL-11), known to downregulate several inflammatory modulators, has the ability in subcutaneous administration to reduce the rate and/or extent of periodontal attachment loss and radiographic bone loss in a ligature-induced periodontal disease beagle dog model.


METHODS
Twenty 18-month-old female beagle dogs were brought to optimal periodontal health over a 2-week period. Periodontal disease was induced by placing 2.0 silk ligatures around the mandibular first molar and premolar teeth. The dogs were divided into 3 treatment groups and one control group. The 3 treatment groups received subcutaneous injections of either 15, 30, or 80 microg/kg of rhIL-11 in saline buffer twice a week. The placebo group received buffer only subcutaneously twice a week. The gingival health of each animal was measured by recording the presence or absence of gingival inflammation, plaque, and bleeding upon probing. Attachment levels and bone height were also measured. Treatment administration and clinical and radiographic evaluations were performed in a masked fashion.


RESULTS
At week 8, the placebo group had 3.89 mm of attachment loss and 73.8% radiographic bone remaining. The 15 microg/kg group had 1.99 mm attachment loss and 89.5% bone remaining; the 30 microg/kg group had 0.84 mm attachment loss and 92.5% bone remaining; and the 80 microg/kg group had 1.05 mm attachment loss and 85.5% bone remaining. All 3 treatment groups lost significantly less attachment and retained significantly more bone than did the placebo group.


CONCLUSIONS
The study indicates that subcutaneous injections of rhIL-11 were able to slow the progression of attachment and radiographic alveolar bone loss in a ligature-induced beagle dog model.
Martuscelli
G
G
Department of Periodontology, Harvard School of Dental Medicine, Boston, MA 02115, USA.
Fiorellini
J P
JP
Crohin
C C
CC
Howell
T H
TH
D016301:Alveolar Bone Loss / Q000000981:diagnostic imaging / Q000517:prevention & control; D000818:Animals; D001641:Bicuspid; D016009:Chi-Square Distribution; D003773:Dental Plaque / Q000145:classification; D004195:Disease Models, Animal; D018450:Disease Progression; D004285:Dogs; D015536:Down-Regulation; D005260:Female; D005884:Gingival Hemorrhage / Q000145:classification; D005891:Gingivitis / Q000145:classification; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007279:Injections, Subcutaneous; D017370:Interleukin-11 / Q000008:administration & dosage / Q000627:therapeutic use*; D008963:Molar; D015588:Observer Variation; D017622:Periodontal Attachment Loss / Q000517:prevention & control; D010510:Periodontal Diseases / Q000276:immunology / Q000382:microbiology / Q000517:prevention & control*; D010518:Periodontitis / Q000517:prevention & control; D010919:Placebos; D011859:Radiography; D011897:Random Allocation; D011994:Recombinant Proteins; D016037:Single-Blind Method
D018836:Inflammation Mediators; D017370:Interleukin-11; D010919:Placebos; D011994:Recombinant Proteins