A New Way to Model Periodontitis in Laboratory Animals

Abstract

The prevalence of periodontal diseases is increasing, tends to increase with age and is considered as one of the main causes of tooth loss. To assess the effectiveness of new methods of treatment of periodontal diseases, studies on laboratory animals can be promising.

The aim of the study: to develop a new method of accelerated modeling of experimental periodontitis on laboratory animals.

Material and methods: The study was carried out on 22 female rats. A wire ligature was applied to the cervical area of the incisors of the animals in an eight-shaped manner. Plaque obtained from a patient with periodontitis was placed under the wire, and nicotine and ethyl alcohol solutions were injected under the gingival mucosa. A complex index has been proposed to assess inflammation. At the end of the experiment the animals were euthanized, their jaws were dissected into dentoalveolar blocks and further descriptive histologic analysis was performed.

Results: On the second day the gingiva of the rats acquired a cyanotic-pink color, on the fourth day the consistency of the gingiva became friable, mobility appeared in the lower incisors. Complex index of inflammation in animals of the main group: before the study-9, on the 7th day-195. Gingival preparations showed signs of exudative inflammation. In alveolar processes-irreversible resorption of bone structures. The difference of indicators in animals before and after the experiment was statistically significant (p < 0.05).

Conclusion: The new experimental model of periodontitis is reproduced in a short period of time, provides intensive development of inflammation, leads to disruption of the integrity of epithelial and connective tissue attachment, destruction of alveolar bone.

Keywords: animal model; experimental induced periodontitis; histologic analysis; inflammation.

Figure 1

Cyanotic appearance of the gingival mucosa in the low incisor region of a rat after the injection was performed.

Figure 2

Inflammation in rat periodontal tissues, hematoxylin and eosin (magnification ×10): I—dentin of the tooth root; II—connective epithelium; III—dental alveolus with detached mucous laminae; IV—fibrinoid swelling of gingival fibers; V—detachment and irregular thinning of sulcular epithelium; VI—smoothed ridges of the basal layer of the gingival epithelium.

Figure 3

Exudative inflammation of rat gingival tissue: macrophage reaction in the mucosal lamina, hematoxylin and eosin (magnification ×100): I—edema-swelling, disorientation of collagen fibers; II—the beginning of leukocyte infiltration of the tissue; III—dilatation of the venule with parietal standing of macrophages; IV—macrophage in the cross section of the capillary; V—accumulation of leukocytes in the capillaries (longitudinal section of the vessel)).

Figure 4

Purulent inflammation of rat gingival tissue, hematoxylin and eosin (magnification ×40): I—drain foci of purulent exudate; II—erythrocyte infiltration: translucent erythrocytes (red) are visible on the section, delimited by a leukocyte shaft; III—leukocyte infiltration.

Figure 5

Granulation tissue overgrowth with inflammatory infiltration in rat gingival tissue, hematoxylin and eosin (magnification ×40): I—pronounced proliferation of fibroblasts; II—signs of collagenogenesis.

Figure 6

Tectorial epithelium of rat gingiva, hematoxylin and eosin (magnification ×10): AB—alveolar bone; ABC—alveolar bone crest; G—gingiva; I—fibrinoid swelling of the gingival connective tissue; II—obstruction-free collagen fibers.

Figure 7

Irreversible osteoclastic resorption of rat alveolar bone structures, hematoxylin and eosin (×10 magnification): AB—alveolar bone; ABC—alveolar bone crest; G—gingiva; CEJ—cementoenamel junction; yellow border—irreversible osteoclastic resorption; PDL—periodontal ligament.