Effects of glucocorticoid-induced osteoporosis on bone tissue of rats with experimental periodontitis
Introduction
Periodontitis is an infectious-inflammatory and highly prevalent disease, characterized by destruction of connective tissue and alveolar bone loss (ABL), and it is considered the second major cause of tooth loss (Tatakis and Kumar, 2005). This disease is mainly initiated by oral biofilm, however the development of an altered host response plays an important role on tissue breakdown (Pihlstrom, Michalowicz, & Johnson, 2005).
Osteoporosis is a common disease characterized by systemic bone loss and impaired bone microarchitecture. It can be a consequence of hormonal imbalance in postmenopausal woman (Jilka, Hangoc, Girasole, Passeri, & Williams, 1992), but it also can present a secondary cause, mainly as a result of the use of some drugs, such as Glucocorticoids (GCs). Glucocorticoid-induced osteoporosis (GIOP) is the most common cause of secondary osteoporosis, the first cause before 50 years of age and the first iatrogenic cause of the disease (Kok & Sambrook, 2009). In addition, considering the continuous raise on the prevalence of GCs use in the community population (Overman, Yeh, & Deal, 2013), it seems interesting to understand the biological mechanisms underlying GIOP.
In the recent decades, numerous studies have focused on the association between osteoporosis and periodontitis at the bone level. The majority of the studies has focused on the effects of postmenopausal osteoporosis on the loss of periodontal attachment (Hernández-Vigueras et al., 2015, Juluri et al., 2015). However, little is known about the effects of GIOP on periodontal tissues. One study showed that GCs can induce an alveolar bone loss in long-term (28 days) treated mice (Bouvard, Gallois, Legrand, Audran, & Chappard, 2013) and another one reported a reduction of bone density in the region of interalveolar septa, insignificant bone tissue loss of the horizontal type and pathological teeth mobility in periodontal tissues of patients with systemic osteoporosis (Dmitrieva, Atrushkevich, & Pikhlak, 2006). There is no study evaluating the effect of GIOP when the periodontal inflammation is present. In this context, we aimed to evaluate the effects of GIOP on bone tissue of rats with experimental periodontitis.
Section snippets
Animals and study design
The experiments were performed on forty-eight young adult male (from two litters) Wistar rats (Rattus norvegicus) from central Animal Facility of Federal University of Ceará, weighing 180–220 g, kept in appropriate cages with six animals each. The animals were housed in standard conditions (12 h light-dark cycles and temperature-controlled rooms) with food and water ad libitum. The protocols for experimental procedures and animal treatment were approved by Animal Ethics Committee (number 78/2014)
Macroscopic, radiographic and micro-computed tomographic (CT) analyses of alveolar bone
On the macroscopic analysis of hemimaxillae (Fig. 1A), Naïve group (Fig. 1C) presented ABL close to zero, i.e. Ligatures for eleven days caused a significant (p < 0.05) ABL in group EP, which presented furcation lesions and root exposure, when compared to group Naïve (Fig. 1E). The response of the rats to GIOP (Fig. 1G) was similar to that of the rats of the Naïve group. However, rats subjected to GIOP + EP (Fig. 1I) showed greater (p < 0.05) ABL when compared to group EP.
The results of the
Discussion
There has been an increase in the use of animal models in studies of initiation and progression of bone diseases, such as osteoporosis and periodontal disease. The ligature-induced periodontitis model has been used extensively as a highly reproducible model that evaluates the progression of periodontitis (Bezerra et al., 2000, Goes et al., 2014, Leitão et al., 2005). As with human periodontitis, experimentally induced periodontitis in rats involves inflammatory cell recruitment with
Conclusion
In summary, within the limits of the present study, we conclude that GIOP can potentiate the destructive effects of experimental periodontitis on alveolar bone of rats and alter their systemic bone loss, by promoting bone resorption and reducing osteoblast activity. Nevertheless, more studies are necessary in order to better understand the biochemical mechanisms of GCs in bone cells during inflammatory conditions.
Conflict of interests
The authors have no conflict of interest to disclose.
Fundings
This study was supported by grants from CNPq and FUNCAP and by the authors themselves.
Ethical approval
The experimental procedures described here were approved by the Institutional Animal Care and Use Committee (#78/2014) and performed in accordance with the Animal Care Standards of Federal University of Ceará.
Acknowledgments
The authors gratefully thank Socorro França Monte of the Department of Morphology, Faculty of Medicine, Federal University of Ceará, Ceará, Brazil, for technical assistance.
References (37)
- et al.
Glucocorticoids reduce alveolar and trabecular bone in mice
Joint Bone Spine
(2013) - et al.
Secondary osteoporosis in patients with an osteoporotic fracture
Best Practice & Research Clinical Rheumatology
(2009) - et al.
Favourable effects of Bacillus subtilis and Bacillus licheniformis on experimental periodontitis in rats
Archives of Oral Biology
(2016) - et al.
Periodontal diseases?
Lancet
(2005) - et al.
Bone alkaline phosphatase in CKD-mineral bone disorder
American Journal of Kidney Disease
(2013) - et al.
Etiology and pathogenesis of periodontal diseases?
Dental Clinics of North America
(2005) - et al.
Analysis of heat inactivation curves of alkaline phosphatase isoenzymes in serum
Clinica Chimica Acta
(1975) - et al.
The effects of tumour necrosis factor-α on bone cells involved in periodontal alveolar bone loss; osteoclasts, osteoblasts and osteocytes
Journal of Periodontal Research
(2016) - et al.
Selective cyclooxygenase-2 inhibition prevents alveolar bone loss in experimental periodontitis in rats
Journal of Periodontology
(2000) - et al.
Low-dose doxycycline prevents inflammatory bone resorption in rats
Brazilian Journal of Medical and Biological Research
(2002)