**4. The implications of the IL-1α and IL-1β cytokines in patients with periodontal disease and osteoporosis**

IL-1α and IL-1β are biologically more or less equivalent pleiotropic factors that act locally and systemically. Only a few functional differences between the factors have been described; only IL-1β appears to be constitutively expressed in the brain. Interleukin-1 is a potent stimulator of bone resorption in vivo; IL-1β has been shown to be the most potent stimulator of bone resorption in vitro. The mechanism by which IL-1β stimulates resorption involves the expression of RANKL in osteoblasts and indirect stimulation of osteoclastogenesis and bone resorption [23].

There are also indications that osteoclasts express interleukin-1 receptor I, which is important for osteoclast activity and survival by activating the PI3K/AKT and ERK pathways, a MyD88-dependent response, but not on TRIF [24].

We conducted a study of 38 postmenopausal female subjects with the purpose to investigate differences in IL-1α and 1β levels in GCF in patients with chronic periodontitis, with or without associated chronic disease (in the present study osteoporosis) [25].

IL-1α was the most prevalent cytokine found in GCF and was detected in all sites studied. We noticed significantly higher differences in interleukin levels for the study group (patients with osteoporosis) compared to systemically healthy patients (p < 0.05).

In order to establish the possible clinical relevance of these observations, a correlation analysis was performed between the clinical parameters and the total levels of cytokines in the test sites. Positive correlations were observed between IL-1α and 1β levels with PPD and CAL [25].

In periodontal inflammation, IL-1β is mainly expressed by macrophages and dendritic cells, but gingival fibroblasts, periodontal ligament cells, and osteoblasts can also secrete IL-1β. Elevated levels of IL-1β as well as IL-1α in gingival crevicular fluid have been reported by several groups [26]. There are many clinical studies showing the importance of IL-1β for inflammation and destruction in rheumatoid arthritis and osteoarthritis, associated with periodontal damage [27].

#### *The Role of Osteoporosis as a Systemic Risk Factor for Periodontal Disease DOI: http://dx.doi.org/10.5772/intechopen.96800*

There are several reasons to believe that IL-1β could be an important mediator of the destruction of gingival connective tissue and periodontal ligament, as well as the resorption of alveolar bone. IL-1β is a potent stimulator of matrix metalloproteinase expression in fibroblasts and periodontal ligament cells [28].

The challenge in osteoimmunology is to determine the relative contribution of various components of the immune system to bone loss induced by ovariectomy and senile osteoporosis. These may also involve identical adjustment paths; however, in each system, there will be subtle differences in the net balance of local or systemic regulators, resulting in specific patterns of subsequent bone loss.
