Regulation of Periodontal Ligament Cell Functions by Interleukin-1β

Abstract

Periodontal ligament (PDL) cells maintain the attachment of the tooth to alveolar bone. These cells reside at a site in which they are challenged frequently by bacterial products and proinflammatory cytokines, such as interleukin-1β (IL-1β), during infections. In our initial studies we observed that IL-1β down-regulates the osteoblast-like characteristics of PDL cells in vitro. Therefore, we examined the functional significance of the loss of the PDL cell’s osteoblast-like characteristics during inflammation. In this report we show that, during inflammation, IL-1β can modulate the phenotypic characteristics of PDL cells to a more functionally significant lipopolysaccharide (LPS)-responsive phenotype. In a healthy periodontium PDL cells exhibit an osteoblast-like phenotype and are unresponsive to gram-negative bacterial LPS. Treatment of PDL cells with IL-1β inhibits the expression of their osteoblast-like characteristics, as assessed by the failure to express transforming growth factor β1 (TGF-β1) and proteins associated with mineralization, such as alkaline phosphatase and osteocalcin. As a consequence of this IL-1β-induced phenotypic change, PDL cells become responsive to LPS and synthesize proinflammatory cytokines. The IL-1β-induced phenotypic changes in PDL cells were transient, as removal of IL-1β from PDL cell cultures resulted in reacquisition of their osteoblast-like characteristics and lack of LPS responsiveness. The IL-1β-induced phenotypic changes occurred at concentrations that are frequently observed in tissue exudates during periodontal inflammation (0.05 to 5 ng/ml). The results suggest that, during inflammation in vivo, IL-1β may modulate PDL cell functions, allowing PDL cells to participate directly in the disease process by assuming LPS responsiveness at the expense of their normal structural properties and functions.

A central role for nuclear factor‐κB pathway in the antiinflammatory and proinflammatory actions of mechanical strain

“…Human PDL cells were isolated, cloned, and cultured in RPMI-1640 supplemented with 10% defined fetal calf serum (FCS) (Hyclone Laboratories, Logan, UT), 2 mM glutamine, 100 U/ml penicillin, and 100 µg/ml streptomycin, following University of Pittsburgh Institutional Review Board approval (22). PDL cell clones, designated as PL-150 and PL-75 (from white females, both 18 years of age) and PL-484 (from a white male, age 22 years), retained their osteoblast-like phenotype between 6th and 12th passages as shown by the presence of alkaline phosphatase, the formation of calcium phosphate nodules, expression of mRNA for TGF-β1 and osteocalcin, and parathyroid hormone-induced cAMP formation, as described previously (22). No significant differences in alkaline phosphatase activity and calcium phosphate nodule formation were observed between these passages (6,22).…”

Increase of CD26/Dipeptidyl Peptidase IV Expression on Human Gingival Fibroblasts upon Stimulation with Cytokines and Bacterial Components

“…The mean fluorescence values were also correlated to the percent positivity of CD26. It has been reported that the phenotypic characteristics of fibroblasts depend on the organs or tissues from which the fibroblasts are derived (1,2,29,31). These results suggested organ specificity in respect to CD26 expression on fibroblasts.…”

Salivary and serum enzymes as diagnostic biomarkers in patients with periodontal disease

“…the salivary enzymatic activity of alp significantly decreases during periodontal ligament attachment loss and bone resorption. release of cytokines (il-1β) during bone resorption may inhibit proliferation of periodontal ligament cells such as osteoblasts (12). the ldh level was also significantly decreased in the saliva of patients with periodontal disease compared to healthy patients group.…”