| Početna strana | Uredništvo | Časopis  | Uputstvo autorima  | Kodeks u  kliničkom i eksperimentalnom radu | Kontakt  |  
| Home page | Editorial  board | About the Journal | Instructions for Authors | Peer Review Policy | Clinical and Experimental Work Code | Contact  |


Acta Medica Medianae
Vol. 51, No 4, December, 2012

UDK 61
ISSN 0365-4478(Printed version)
ISSN 1821-2794(Online)


Correspondence to:

Milica Petrović

Clinic of Dentistry

Department of Prosthodontics

Bul. dr Zorana Đinđića 52, Niš, Serbia

E-mail: petrovicmilica21@gmail.com

Review article                                            

UDC: 616-097:[ 616.314+616.71-007.234






Milica Petrović1,, Snežana Cekić3, Zorica Ajduković1,2, Marija Medarov4,

 Miloš Kostić4 and Nadica Đorđević5



                     Clinic of  Dentistry, Department of Prosthodontics, Niš, Serbia1

                     University of Nis, Faculty of Medicine, Niš, Serbia2

                     University of Niš, Department of Physiology, Faculty of Medicine, Niš, Serbia3

                     University of Niš,  Department of Immunology, Faculty of Medicine, Niš, Serbia4

                     Clinic of Dentistry, Department of Prosthodontics, Faculty of Medicine, University of Pristina,Kosovska Mitrovica, Serbia5



Osteoporosis and periodontitis are widespread diseases among male and female population, whose incidence increases with aging. The basic pathogenic mechanism of osteoporosis and periodontal disease is a bone resorption with increased production of proinflammatory cytokines: interleukin IL-1β, IL-6, TNF-α and RANKL. The discovery of receptor activator of NF-κB (RANK), its ligand (RANKL) and osteoprotegerin (OPG) has contributed to the understanding of bone biology and mechanisms of osteoclastogenesis. RANKL-RANK interaction is critical for differentiation and maintenance of osteoclast activity. The balance between RANKL and OPG regulates osteoclastogenesis, and thus bone resorption. The disruption of the RANKL/RANK/OPG axis leads to an imbalance between bone formation and bone resorption; therefore, it is responsible for the disturbed bone homeostasis. Loss of bone density associated with decreased estrogen levels is the result of a significant increase in osteoclast activity. Menopausal bone loss may be the result of osteoclast overactivation by proinflammatory cytokines and it is associated with reduced estrogen levels. The lack of estrogen can lead to worsening of periodontal disease and it increases the rate of the gingival connective tissue damage by stimulating the synthesis of several cytokines responsible for bone resorption. Cytokines and RANKL/OPG signaling pathway involved in the pathogenesis of osteoporosis and periodontal disease can lead to the activation of osteoclasts and the stimulation of bone resorption. These findings in the future may improve the usual treatment of periodontal disease and osteoporosis therapy, including the inhibition of proinflammatory mediators and osteoclast activity with the additional use of anti-inflammatory drugs. This involves blocking the binding of different stimulating factors to their receptors on osteoclast precursors, particularly RANKL and development of new more selective drugs with fewer side effects that would act as an anti-cytokines preventing the binding of cytokines to their receptors. Acta Medica Medianae 2012;51(4):51-57.


      Key words: postmenopausal osteoporosis, periodontal disease, inflammation, cytokines