osteoprotegerin and Pulpitis

To summarize the collective in vitro, in vivo and clinical evidence of the involvement of the receptor activator of NF-κB ligand (RANKL)-osteoprotegerin (OPG) system, a system of two molecules controlling osteoclast differentiation and hard-tissue resorption, in pulpal and periapical pathophysiology.. A systematic search related to RANKL and/or OPG and pulp or periapical disease was conducted on Medline, Biosis, Cochrane, Embase and Web of Science databases using keywords and controlled vocabulary. No language restriction was applied. Two independent reviewers first screened titles and abstracts and then the full texts that were initially included. The reference lists of the identified publications were examined for additional titles.. A total of 33 papers were identified. In vitro studies (N = 11) revealed that pulpal cells can be stimulated by various inflammatory agents to produce RANKL, whilst many studies did not consider the RANKL/OPG ratio. Animal studies (N = 9) mostly focused on the time course and development of periapical lesions in relation to the RANKL-OPG system. Levels of RANKL and OPG in the necrotizing pulp were not investigated. Human studies (N = 13) showed a steady-state expression of OPG in the odontoblast layer. Conflicting results have been reported regarding the role of RANKL in active apical periodontitis, again because the correlation of this molecule with its inhibitor (OPG) was often disregarded.. There is relatively little information currently available that would highlight the specific role of RANKL and OPG in pulpal and periapical disease. OPG may play a protective role against internal resorption, whilst an increased periapical RANKL/OPG ratio might indicate bone resorption.

Topics: Alveolar Bone Loss; Animals; Cells, Cultured; Humans; Mice; Odontoblasts; Osteoprotegerin; Periapical Periodontitis; Pulpitis; Rats; Receptor Activator of Nuclear Factor-kappa B

The dental pulp space can become infected due to a breach in the surrounding hard tissues. This leads to inflammation of the pulp (pulpitis), soft tissue breakdown, and finally to bone loss around the root apex (apical periodontitis). The succession of the molecular events leading to apical periodontitis is currently not known. The main inflammatory mediator associated with neutrophil chemotaxis is interleukin-8 (IL-8), and with bone resorption the dyad of receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG). The levels of RANKL, OPG and IL-8 were studied in periapical tissue fluid of human teeth (n = 48) diagnosed with symptomatic irreversible pulpitis (SIP) and asymptomatic apical periodontitis (AAP). SIP represents the starting point, and AAP an established steady state of the disease. Periapical tissue fluid samples were collected using paper points and then evaluated using enzyme-linked immunosorbent assays (ELISAs). Target protein levels per case were calibrated against the corresponding total protein content, as determined fluorometrically. RANKL was expressed at significantly higher levels in SIP compared to AAP (P < 0.05), whereas OPG was under the detection limit in most samples. In contrast, IL-8 levels were significantly lower in SIP compared to AAP (P < 0.05). Spearman's correlation analysis between RANKL and IL-8 revealed a significantly (P < 0.05) negative correlation between the two measures (rho = -.44). The results of this study suggest that, in the development of apical periodontitis, periapical bone resorption signaling, as determined by RANKL, occurs prior to inflammatory cell recruitment signaling, as determined by IL-8.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Bone Resorption; Dental Pulp; Enzyme-Linked Immunosorbent Assay; Female; Humans; Inflammation; Interleukin-8; Male; Middle Aged; Osteoprotegerin; Periapical Periodontitis; Periapical Tissue; Pulpitis; RANK Ligand; Young Adult

This study investigated the expression of osteoprotegerin (OPG) in healthy and inflamed dental pulps. Histological sections 7 microm thick of 47 teeth, either caries-free or affected by gross caries, were used. Sections were stained with hematoxylin-eosin, and other sections of the same specimen were subjected to the avidin-biotin peroxidase complex immunohistochemical procedure for detection of OPG. The study focused on the coronal pulp that was divided into peripheral and central regions. In the peripheral pulp healthy and inflamed specimens showed high OPG immunoreactivity of the odontoblastic layer. When no inflammation was present in the central pulp OPG immunoreactivity was light. Fibroblasts and endothelial cells showed immunoreactivity ranging from none to intense. When inflammation was present in the central pulp the chronic inflammatory cells showed intense immunoreactivity.

Topics: Chi-Square Distribution; Coloring Agents; Dental Caries; Dental Pulp; Endothelium, Vascular; Eosine Yellowish-(YS); Fibroblasts; Fluorescent Dyes; Glycoproteins; Hematoxylin; Humans; Immunoenzyme Techniques; Immunohistochemistry; Lymphocytes; Macrophages; Odontoblasts; Osteoprotegerin; Pulpitis; Receptors, Cytoplasmic and Nuclear; Receptors, Tumor Necrosis Factor