Evaluation of galectin-3, peptidylarginine deiminase-4, and tumor necrosis factor-α levels in gingival crevicular fluid for periodontal health, gingivitis, and Stage III Grade C periodontitis: A pilot study.
galectin 3
gingival crevicular fluid
periodontal diseases
protein-arginine deiminases
Journal
Journal of periodontology
ISSN: 1943-3670
Titre abrégé: J Periodontol
Pays: United States
ID NLM: 8000345
Informations de publication
Date de publication:
01 2022
01 2022
Historique:
revised:
23
04
2021
received:
10
03
2021
accepted:
23
04
2021
pubmed:
30
4
2021
medline:
3
5
2022
entrez:
29
4
2021
Statut:
ppublish
Résumé
Comparing the gingival crevicular fluid (GCF) levels of galectin-3, peptidylarginine deiminase 4 (PAD4) and tumor necrosis factor-alpha (TNF-α) in individuals with stage III grade C periodontitis and gingivitis and with healthy periodontium was the purpose of this clinical research. Sixty systemically healthy and non-smoker individuals consisting of stage III grade C periodontitis (group S3P/n = 20), gingivitis (group G/n = 20), and periodontally healthy (group HP/n = 20) were recruited for this research. Clinical parameters such as probing depth, clinical attachment level, gingival index, plaque index, and bleeding on probing were recorded in periodontal charts. Enzyme-linked immunosorbent assay method was used in evaluating the GCF levels of galectin-3, PAD4, and TNF-α for study groups. The GCF galectin-3 total amount was highest in group S3P compared with group G and group HP (P <0.05). Its total amount was also higher in group G compared with group HP (P <0.05). The GCF PAD4 total amount was higher in group S3P compared with group HP (P <0.05) but was similar with group G (P >0.05). Its total amounts were also similar in group G and group HP (P >0.05). The GCF TNF-α total amounts were similar in group S3P and group G (P >0.05) but significantly greater than the group HP (P ˂0.05). The GCF galectin-3, PAD4, and TNF-α concentrations were lower in the group S3P and group G compared with the group HP (P <0.05). There were significant positive correlations between GCF galectin-3 total amount and all clinical parameters (P ˂0.01) and also between GCF galectin-3 and TNF-α total amounts (P ˂0.01). There was no correlation between PAD4 and clinical parameters, or between PAD4 and TNF-α (P >0.05). Galectin-3 and PAD4 may be involved in the periodontal disease pathogenesis considering the elevated levels of these molecules in periodontal disease. These biomarkers may be used in the diagnosis of periodontal diseases.
Sections du résumé
BACKGROUND
Comparing the gingival crevicular fluid (GCF) levels of galectin-3, peptidylarginine deiminase 4 (PAD4) and tumor necrosis factor-alpha (TNF-α) in individuals with stage III grade C periodontitis and gingivitis and with healthy periodontium was the purpose of this clinical research.
METHODS
Sixty systemically healthy and non-smoker individuals consisting of stage III grade C periodontitis (group S3P/n = 20), gingivitis (group G/n = 20), and periodontally healthy (group HP/n = 20) were recruited for this research. Clinical parameters such as probing depth, clinical attachment level, gingival index, plaque index, and bleeding on probing were recorded in periodontal charts. Enzyme-linked immunosorbent assay method was used in evaluating the GCF levels of galectin-3, PAD4, and TNF-α for study groups.
RESULTS
The GCF galectin-3 total amount was highest in group S3P compared with group G and group HP (P <0.05). Its total amount was also higher in group G compared with group HP (P <0.05). The GCF PAD4 total amount was higher in group S3P compared with group HP (P <0.05) but was similar with group G (P >0.05). Its total amounts were also similar in group G and group HP (P >0.05). The GCF TNF-α total amounts were similar in group S3P and group G (P >0.05) but significantly greater than the group HP (P ˂0.05). The GCF galectin-3, PAD4, and TNF-α concentrations were lower in the group S3P and group G compared with the group HP (P <0.05). There were significant positive correlations between GCF galectin-3 total amount and all clinical parameters (P ˂0.01) and also between GCF galectin-3 and TNF-α total amounts (P ˂0.01). There was no correlation between PAD4 and clinical parameters, or between PAD4 and TNF-α (P >0.05).
CONCLUSIONS
Galectin-3 and PAD4 may be involved in the periodontal disease pathogenesis considering the elevated levels of these molecules in periodontal disease. These biomarkers may be used in the diagnosis of periodontal diseases.
Identifiants
pubmed: 33913157
doi: 10.1002/JPER.21-0137
doi:
Substances chimiques
Galectin 3
0
TNF protein, human
0
Tumor Necrosis Factor-alpha
0
PADI4 protein, human
EC 3.5.3.15
Protein-Arginine Deiminase Type 4
EC 3.5.3.15
Protein-Arginine Deiminases
EC 3.5.3.15
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
80-88Informations de copyright
© 2021 American Academy of Periodontology.
Références
Buduneli N, Kinane DF. Host-derived diagnostic markers related to soft tissue destruction and bone degradation in periodontitis. J Clin Periodontol. 2011;38(suppl 11):85-105.
Hara A, Niwa M, Kanayama T, et al. Galectin-3: a potential prognostic and diagnostic marker for heart disease and detection of early stage pathology. Biomolecules. 2020,10:1277.
Sciacchitano S, Lavra L, Morgante A, et al. Galectin-3: one molecule for an alphabet of diseases, from a to z. Int J Mol Sci. 2018;19:379.
Dong R, Zhang M, Hu Q, et al. Galectin-3 as a novel biomarker for disease diagnosis and a target for therapy (Review). Int J Mol Med. 2018;41:599-614.
Hara A, Niwa M, Noguchi K, et al. Galectin-3 as a next-generation biomarker for detecting early stage of various diseases. Biomolecules. 2020:10.
Issa SF, Duer A, Ostergaard M, et al. Increased galectin-3 may serve as a serologic signature of pre-rheumatoid arthritis while markers of synovitis and cartilage do not differ between early undifferentiated arthritis subsets. Arthritis Res Ther. 2017;19:80.
Li S, Yu Y, Koehn CD, Zhang Z, Su K. Galectins in the pathogenesis of rheumatoid arthritis. J Clin Cell Immunol. 2013;4.
Ohshima S, Kuchen S, Seemayer CA, et al. Galectin 3 and its binding protein in rheumatoid arthritis. Arthritis Rheum. 2003;48:2788-2795.
Dasuri K, Antonovici M, Chen K, et al. The synovial proteome: analysis of fibroblast-like synoviocytes. Arthritis Res Ther. 2004;6:R161-168.
Neidhart M, Zaucke F, von Knoch R, et al. Galectin-3 is induced in rheumatoid arthritis synovial fibroblasts after adhesion to cartilage oligomeric matrix protein. Ann Rheum Dis. 2005;64:419-424.
Shou J, Bull CM, Li L, et al. Identification of blood biomarkers of rheumatoid arthritis by transcript profiling of peripheral blood mononuclear cells from the rat collagen-induced arthritis model. Arthritis Res Ther. 2006;8:R28.
Forsman H, Islander U, Andreasson E, et al. Galectin 3 aggravates joint inflammation and destruction in antigen-induced arthritis. Arthritis Rheum. 2011;63:445-454.
Gruszewska E, Cylwik B, Gindzienska-Sieskiewicz E, Kowal-Bielecka O, Mroczko B, Chrostek L. Diagnostic power of galectin-3 in rheumatic diseases. J Clin Med. 2020;9.
Vossenaar ER, Zendman AJ, van Venrooij WJ, Pruijn GJ. PAD, a growing family of citrullinating enzymes: genes, features and involvement in disease. Bioessays. 2003;25:1106-1118.
Baka Z, Gyorgy B, Geher P, Buzas EI, Falus A, Nagy G. Citrullination under physiological and pathological conditions. Joint Bone Spine. 2012;79:431-436.
Meyer O, Labarre C, Dougados M, et al. Anticitrullinated protein/peptide antibody assays in early rheumatoid arthritis for predicting five year radiographic damage. Ann Rheum Dis. 2003;62:120-126.
Zendman AJ, Vossenaar ER, van Venrooij WJ. Autoantibodies to citrullinated (poly)peptides: a key diagnostic and prognostic marker for rheumatoid arthritis. Autoimmunity. 2004;37:295-299.
Nesse W, Westra J, van der Wal JE, et al. The periodontium of periodontitis patients contains citrullinated proteins which may play a role in ACPA (anti-citrullinated protein antibody) formation. J Clin Periodontol. 2012;39:599-607.
Damgaard D, Senolt L, Nielsen CH. Increased levels of peptidylarginine deiminase 2 in synovial fluid from anti-CCP-positive rheumatoid arthritis patients: association with disease activity and inflammatory markers. Rheumatology. 2016;55:918-927.
Laugisch O, Wong A, Sroka A, et al. Citrullination in the periodontium-a possible link between periodontitis and rheumatoid arthritis. Clin Oral Investig. 2016;20:675-683.
Engstrom M, Eriksson K, Lee L, et al. Increased citrullination and expression of peptidylarginine deiminases independently of P. gingivalis and A. actinomycetemcomitans in gingival tissue of patients with periodontitis. J Transl Med. 2018;16:214.
Janssen KMJ, de Smit MJ, Withaar C, et al. Autoantibodies against citrullinated histone H3 in rheumatoid arthritis and periodontitis patients. J Clin Periodontol. 2017;44:577-584.
Graves DT, Cochran D. The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction. J Periodontol. 2003;74:391-401.
Nishikawa M, Yamaguchi Y, Yoshitake K, Saeki Y. Effects of TNFalpha and prostaglandin E2 on the expression of MMPs in human periodontal ligament fibroblasts. J Periodontal Res. 2002;37:167-176.
Chapple ILC, Mealey BL, Van Dyke TE, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: consensus report of workgroup 1 of the 2017 World Workshop on the classification of periodontal and peri-implant diseases and conditions. J Clin Periodontol. 2018;45(suppl 20):S68-S77.
Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: consensus report of workgroup 2 of the 2017 World Workshop on the classification of periodontal and peri-implant diseases and conditions. J Clin Periodontol. 2018;45(suppl 20):S162-S170.
Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: framework and proposal of a new classification and case definition. J Clin Periodontol. 2018;45(suppl 20):S149-S161.
Tonetti MS, Sanz M. Implementation of the new classification of periodontal diseases: decision-making algorithms for clinical practice and education. J Clin Periodontol. 2019;46:398-405.
Silness J, Loe H. Periodontal disease in pregnancy. Ii. correlation between oral hygiene and periodontal condition. Acta Odontol Scand. 1964;22:121-135.
Loe H. The gingival index, the plaque index and the retention index systems. J Periodontol. 1967;38(suppl):610-616.
Gokul K, Faizuddin M, Pradeep AR. Estimation of the level of tumor necrosis factor- alpha in gingival crevicular fluid and serum in periodontal health & disease: a biochemical study. Indian J Dent Res. 2012;23:348-352.
Lamster IB, Oshrain RL, Gordon JM. Enzyme activity in human gingival crevicular fluid: considerations in data reporting based on analysis of individual crevicular sites. J Clin Periodontol. 1986;13:799-804.
Iacobini C, Blasetti Fantauzzi C, Bedini R, et al. Galectin-3 is essential for proper bone cell differentiation and activity, bone remodeling and biomechanical competence in mice. Metabolism. 2018;83:149-158.
Filer A, Bik M, Parsonage GN, et al. Galectin 3 induces a distinctive pattern of cytokine and chemokine production in rheumatoid synovial fibroblasts via selective signaling pathways. Arthritis Rheum. 2009;60:1604-1614.
Uchino Y, Woodward AM, Mauris J, et al. Galectin-3 is an amplifier of the interleukin-1beta-mediated inflammatory response in corneal keratinocytes. Immunology. 2018;154:490-499.
Yamaoka A, Kuwabara I, Frigeri LG, Liu FT. A human lectin, galectin-3 (epsilon bp/Mac-2), stimulates superoxide production by neutrophils. J Immunol. 1995;154:3479-3487.
Gittens BR, Bodkin JV, Nourshargh S, Perretti M, Cooper D. Galectin-3: a positive regulator of leukocyte recruitment in the inflamed microcirculation. J Immunol. 2017;198:4458-4469.
Iacobini C, Fantauzzi CB, Pugliese G, Menini S. Role of galectin-3 in bone cell differentiation, bone pathophysiology and vascular osteogenesis. Int J Mol Sci. 2017;18:2481.
Li YJ, Kukita A, Teramachi J, et al. A possible suppressive role of galectin-3 in upregulated osteoclastogenesis accompanying adjuvant-induced arthritis in rats. Lab Invest. 2009;89:26-37.
Lee YJ, Kang SW, Song JK, et al. Serum galectin-3 and galectin-3 binding protein levels in Behcet's disease and their association with disease activity. Clin Exp Rheumatol. 2007;25:S41-45.
Miyauchi M, Ao M, Furusho H, et al. Galectin-3 plays an important role in preterm birth caused by dental infection of Porphyromonas gingivalis. Sci Rep. 2018;8:2867.
Harvey GP, Fitzsimmons TR, Dhamarpatni AA, Marchant C, Haynes DR, Bartold PM. Expression of peptidylarginine deiminase-2 and -4, citrullinated proteins and anti-citrullinated protein antibodies in human gingiva. J Periodontal Res. 2013;48:252-261.
Knuckley B, Causey CP, Jones JE, et al. Substrate specificity and kinetic studies of PADs 1, 3, and 4 identify potent and selective inhibitors of protein arginine deiminase 3. Biochemistry. 2010;49:4852-4863.
Selvig KA, Zander HA. Chemical analysis and microradiography of cementum and dentin from periodontally diseased human teeth. J Periodontol. 1962;33:303-310.
Tasdemir I, Erbak Yilmaz H, Narin F, Saglam M. Assessment of saliva and gingival crevicular fluid soluble urokinase plasminogen activator receptor (suPAR), galectin-1, and TNF-alpha levels in periodontal health and disease. J Periodontal Res. 2020;55:622-630.
Ebersole JL, Graves CL, Gonzalez OA, et al. Aging, inflammation, immunity and periodontal disease. Periodontol 2000. 2016;72:54-75.