IL-34 Levels in Various Types of Periodontitis
Condition: Chronic Periodontitis; Aggressive Periodontitis
MeSH terms: Periodontitis; Chronic Periodontitis; Aggressive Periodontitis
Study type: Interventional

Summary: 
      The objective of this study is to 1) identification of the impact of IL-34 on the
      pathogenesis of periodontal disease and determine whether any relationship among the existing
      levels of Gingival crevicular fluid (GCF) Interleukin 34( IL-34 )and GCF Receptor activator
      of nuclear factor -kB ligand (RANKL), osteoprotegerin (OPG) and RANKL/OPG ratio, as a
      mediator of bone resorption 2) analysis of the impact of non-surgical periodontal treatment
      on GCF IL-34 levels in patients with chronic periodontitis (CP) and aggressive periodontitis
      (AgP) and 3) to correlate between biochemical markers and clinical recordings
    

Detailed description: 
      A novel cytokine interleukin 34 (IL-34) is a second possible functional ligand of macrophage
      colony-stimulating factor-1 receptor (CSF-1R). IL-34 is secreted in different tissues
      including: heart, brain, lung, liver, kidney, thymus, testes, ovary, small intestine,
      prostate, colon and spleen . IL-34 shares vital functions of macrophage colony-stimulating
      factor -1(CSF-1), and manage myeloid cell survival, differentiation and proliferation. It is
      produced by synovial fluid, gingival fibroblast and human adipose tissue, and is controlled
      by the transcription factor RANK and activation of c-Jun N-terminal kinase (CJNK).
      Additionally, the pro-inflammatory cytokines tumornecrosis factor-alfa (TNF-α) and
      interleukin-1beta (IL-1β) arrange IL-34 release from gingival fibroblasts, by a mechanism
      including nuclear factor -kB (NF-kB) and mitogen activated protein kinase (MAPK).The
      targeting CSF-1 merely is not adequate to inhibit the effect via CSF-1R. Moreover, neither
      RANKL nor IL-34 solely can cause osteoclast formation which suggests that IL-34 is required
      but not enough. IL-34 plays a crucial role in RANKL-induced osteoclastogenesis; the
      osteoclasts differentiation is mediated by the same way with CSF-1.

      Several studies evaluated the role of IL-34 in the pathogenesis of chronic periodontitis
      (CP). To the best of our knowledge, any of these studies reported the relationship between
      GCF IL-34 level and GCF RANKL/OPG ratio in other types of periodontitis before and after
      non-surgical periodontal therapy. This study highlights the influence of IL-34 in the
      pathogenesis of Chronic Periodontitis (CP) and Aggressive Periodontitis (AgP).

      The objective of this study is to 1) identification of the impact of IL-34 on the
      pathogenesis of periodontal disease and determine whether any relationship among the existing
      levels of GCF IL-34 and GCF RANKL, OPG and RANKL/OPG ratio, as a mediator of bone resorption
      2) analysis of the impact of non-surgical periodontal treatment on GCF IL-34 levels in
      patients with CP and AgP and 3) to correlate between biochemical markers and clinical
      recordings.

      The study included 60 subjects: 20 who were periodontally healthy (CTRL), 20 with chronic
      periodontitis (CP)and 20 with aggressive periodontitis (AgP). Patients with periodontitis
      were treated with non-surgical periodontal therapy. GCF sampling procedures and clinical
      periodontal measures were investigated at the baseline and 6 weeks after treatment. Levels of
      IL-34, RANKL and OPG were analyzed with Enzyme-linked immunosorbent assay (ELISA).

      Participants were periodontally assessed at baseline and after non-surgical periodontal
      therapy in accordance with the following criteria; plaque index (PI)(Silness and Loe, 1964),
      GI(Loe and Silness, 1963), PPD, clinical attachment level (CAL) and BOP (judged positive if
      it developed within 15 s following contact). Full-mouth periapical radiographs were used to
      determine the periodontal bone loss.The clinical measurement were taken in millimeters by a
      single calibrated examiner (ŞBD), who was blinded to the whole study composition, from six
      locations of each tooth (mesio-buccal, disto-buccal, mid-buccal, mesiolingual, disto-lingual,
      and mid-lingual), by the use of a periodontal probe (Hu-Friedy, Chicago, IL, USA).

      Two sites per participant were selected to collect GCF for each group. GCF samples were
      collected from the mesiobuccal or distobuccal sites of single-rooted teeth. The sample areas
      were isolated with cotton rolls, saliva contamination was ensured, all supragingival plaque
      was eliminated by sterile curette and it was slightly air dried. The paper strips were
      inserted within the crevice until resistance was encountered and then allowed to remain in
      place for 30 seconds. The amount of GCF on the strips was measured by weighing the collected
      liquid. The strips were placed into closed and numbered plastic eppendorf tubes. The liquid
      was weighed again, immediately after collection, to take into account evaporation. The
      samples consisting of saliva and blood were discarded from the study. Two available for use
      samples from per individual were merged to make a singular sample and instantly insert in a
      singular Eppendorf tube and freezed at _80°C until aftertime evaluation.
    

Intervention name(s): non-surgical periodontal treatment
Intervention type(s): Other
Intervention description(s): scaling and root planing were performed
Allocation: Non-Randomized
Intervention model: Parallel Assignment
Masking: Single (Outcomes Assessor)
Primary purpose: Treatment
Keywords: Periodontitis; Interleukin 34; RANKL; OPG; gingival crevicular fluid