Expression of MRP8/MRP14 mRNA in Monocytes of Periodontitis: Comparison between Diabetic and Non Diabetic Patients

Ahmad Syaify(1*), Sri Budi Barunawati(2), Suryono Suryono(3), Marsetyawan HNES(4)

(1) Universitas Gadjah Mada, Yogyakarta, Indonesia
(2) Universitas Gadjah Mada, Yogyakarta, Indonesia
(3) Universitas Gadjah Mada, Yogyakarta, Indonesia
(4) Universitas Gadjah Mada, Yogyakarta, Indonesia
(*) Corresponding Author


The severity of periodontitis on patients with type 2 Diabetes Mellitus patients was strongly thought caused by decreasing of leukocytes function such as monoctyes and neutrophils. In our previous research it was found that calprotectin (MRP8/MRP14) level in leukocytes of periodontitis patients with type 2 DM was higher than periodontitis in non DM. The aim of this study was to determine calprotectin (MRP8/MRP14)
mRNA expression in human monocytes of periodontitis patients with type 2 DM and without DM. Monocytes were isolated from the peripheral blood of periodontitis patients with uncontrolled type 2 DM, controlled type 2 DM, and non DM. The expression of total RNA calprotectin (MRP8 and MRP14) were detected by RTPCR using GAPDH as the innate control. It was observed that the value of MRP8/MRP14 mRNA expression DM patients were higher than non DM, and the highly significant increase expression (p<0.05) was on the uncontrolled type 2 DM. The basal level of MRP8/MRP14 expression increased in monocyte of periodontitis and type 2 DM patients compared with non diabetes subjects. It was suggested that high basal level MRP8/MRP14 has role in the regulation of severity periodontitis with diabetes mellitus.


MRP8/MRP14, monocytes, periodontitis, type 2 DM

Full Text:



Perkeni. 2001. Konsensus Pengelolaan Diabetes Mellitus Tipe 2 di Indonesia. Jakarta: 1 42.

Arrieate-Blanco JJ, Bartolome-Villar B, Jimenez-Martinez E, Saavedra-Vallejo P. 2003. Dental problems in patients with DM (II): ginginal index and perodontal disease. Med Oral. 8: 233-47.

Depkes RI. 2002. Profil Kesehatan Indonesia 2001: Menuju Indonesia Sehat 2010. Pusat Data Departemen Kesehatan RI, Jakarta.

Mealey B. 2000. Diabetes and periodontal disease: Position Paper. J. Periodontol. 70: 935-49.

Iacopino AM, and Cuttler CW. 2000. Pathophysiological relationship between periodontitis and systemic disease: recent

concept involving serum lipids in periodontitis and systemic disease. J. Periodontol, 71 (8): 1375-84.

Fagerhol MK, Andersson KB, Naess-Andresen C, Brandzaeg C, Dale I. 1990. Calprotectin (The L1 Leukocyte Protein) in Smith, V.L., Dedman J.R, eds. Stimulus Response Coupling: The Role of

Intercellular Calcium-binding Proteins. Boca Raon, CRC Press: 187-210.

Kerkhoff C, Klempt M, Sorg C. Novel insights into Structure and Function of MPR8 (S199A8) and MPR14 (S100A9). Biochem Biophsy Acta 1448: 200-11.

Fagerhol MK. 2000. Calportectin, a faecal marker of organic gastrointestinal abnormality. Lancet 356: 1783-4.

Suryono, Kido J, Hayashi N, Kataoka M, Nagata T. Calprotectin Expresssion in Human Monocytes: Induction by Porphyromonas gingivalis Lipopolysaccharide, Tumor Necrosis Factor-α, and Interleukine-1β. J. Periodontol. 76 : 437-42.

Ahmad Syaify, Marsetyawan, Suryono. Level of Calprotectin ini Serum of Periodontitis Patient with Type 2 Diabetes Mellitus. 2008. Journal of PDGI, Special edition in Congress XXII March

: 1-5.

Ahmad Syaify, Marsetyawan, Sudibyo, Suryono. 2008. Calprotectin mRNA (MRP8/MRP14) expression in neutrophils of periodontitis patients with type 2 diabetes mellitus. Dental Journal 42 (3): 130-3.

Ryan EM, Carnu O, Kamer A. 2003. The Influence of Diabetes on the Periodontal Tissues. J. Am. Dent. Ass 143: 34S – 40S.

Southerland JH, Taylor GW, Offenbacher S. 2005. Diabetes and Periodontal Infection Making the Connection. Clinical Diabetes. 23 (4): 171-8.

Miller LS, Manwell MA, Newbold D. 1992. The Relationship between reduction in Periodontal Inflammation and Diabetes Control: a Report of 9 Cases. J. Periodontol 63 (10): 843-8.

Grossi SG, and Genco RJ. 1998. Periodontal Disease and Diabetes Mellitus: a Two-way Relationships. Annal of Periodontol 3(1): 51 -61.

Suryono, Kido J, Hayashi N, Kataoka M, Shinohara Y, Nagata I. 2006. Noreohineohrin stimulates calprotetcin expression in human monocytes cell. J Periodont Res 41: 159-64.

Little JW, and Falace DA.1988. Dental Management of The Medically Compromised Patient. 3rd Ed. Mosby Co., St. Louis: 291-307.

Hessian PA, Edgeworth J, Hogg N. 1993. MRP-8 and MRP-14, two abundant Ca –binding proteins of neutrophil and monocytes. J. Leukocyte Biol. 53: 197-203.

Miyasaki KT, Bodeua AM, Shafer WM, Pohl J, Murthy RK, Lehrer RI. 1994. New ideas about neutrophil antimicrobial mechanisme: antibiotic peptides, postphagocytic protein processing, and

cytosolic defense factors, in Molecular Pathogenesis of Periodontal Disease. American Society for Microbiol, Washington D.C.: 321-35.

Marhamah. 2004. Pathomechanism of periodontal tissue damage in patients with type 2 diaebets mellitus. Disertation. Hasanuddin University, Makasar, Indonesia.

Graves DT, Liu R, Alikhani M, Al-Mashat H, Trackman PC. 2006. Diabetes-anhanced inflammation and apoptosis: impact on

periodontal pathology. J.Dent Res. 85(1): 15-21.

Suryono, Kido J, Hayashi N, Kataoka M, Nagata T. 2003. Effect of Porphyromonas gingivalis lipopolysaccharide, tumor necrosis factor-alfa and interleukin 1-beta on calprotectin release in

human monocytes. J Periodontol 74: 1719-24.

Kido J, Kido R, Suryono, Kataoka M, Fagerhol MK, Nagata T. 2003. Calprotectin release from human neutrophils is induced by Porphyromonas gingivalis lipopolysaccharide via the CD-14-Toll

like receptor-NFKB pathway. J Periodontol Res 38: 557-63.

Ehlermann P, Eggers K, Bierhaus A, Most P, Weuchenhan D, Greten J, Nawroth PP, Katus HA, Remppis A. 2006. Increased proinflamatory endothelial respons to S100A8/9 after

preactivation through advanced glycation end products. Cardiovascular Diabetology 5(6): 1-9.


Article Metrics

Abstract views : 342 | views : 179


  • There are currently no refbacks.





website statistics


View My Stats