Differences in mucin expression in the submandibular glands of rats during peridontitis induction

Nunuk Purwanti, Banun Kusumawardhani, Kwartarini Murdiastuti

= http://dx.doi.org/10.20473/j.djmkg.v51.i2.p52-56
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Background: Porphyromonas gingivalis (Pg) produces lipopolysacharide (LPS) which acts as a stimulator of inflammation in periodontal tissues. Periodontitis-induced apoptosis and vacuolation of the salivary gland, therefore, causes hyposalivation. Mucin secretion is produced by the submandibular gland under stimulation by the cholinergic and adrenergic receptors. Both forms of stimulation influence the volume of mucin secretion. Mucin saliva plays an important role in the early stages of Pg colonization in the oral cavity. On the other hand, it serves to protect against bacterial invasion. Purpose: The aim of this research was to identify differences in mucin expression in the submandibular gland during periodontitis induction. Methods: 32 male Wistar rats were assigned to either a sham periodontitis or a periodontitis group. The former group received a daily injection of a vehicle solution (n = 16), while members of the periodontitis induction group (n=16) were injected each day with 500 µL of Pg 108 into the mesial area of the upper molar. Mucin in the submandibular gland was analyzed at the 7th, 14th, 21th and 28th days after injection by means of periodic acid schiff (PAS) staining. Results: 28 days after injection mild gingivitis was developed in the periodontitis experiment group. Junctional epithelium (JE) thickness decreased gradually following the increase of PG injection periods (p<0.05).  However, mucin expression increased prominently at 7th, 14th, and 21th days after injection and decreased on day 28th after PG injection. Mucin was expressed in the duct cells of the submandibular gland. Conclusion: The result of this study suggests that there are different levels of mucin expression in the submandibular gland during periodontitis induction.


Porphyromonas gingivalis; periodontitis; mucin

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Yu KM, Inoue Y, Umeda M, Terasaki H, Chen ZY, Iwai T. The peridontal anaerobe Porphyromonas gingivalis induced platelet activation and increased aggregation in whole blood by rat model. Thromb Res. 2011; 127(5): 418–25.

Kim D, Lee G, Huh YH, Lee SY, Park KH, Kim S, Kim J, Koh J, Ryu J. NAMPT is an essential regulator of RA-mediated periodontal inflammation. J Dent Res. 2017; 96(6): 703–11.

Puertas A, Magan-Fernandez A, Blanc V, Revelles L, O’Valle F, Pozo E, León R, Mesa F. Association of periodontitis with preterm birth and low birth weight: a comprehensive review. J Matern Neonatal Med. 2018; 31(5): 597–602.

Han SS, Shin N, Lee SM, Lee H, Kim DK, Kim YS. Correlation between periodontitis and chronic kidney disease in Korean adults. Kidney Res Clin Pract. 2013; 32(4): 164–70.

Otomo-Corgel J, Pucher JJ, Rethman MP, Reynolds MA. State of the science: chronic periodontitis and systemic health. J Evid Based Dent Pract. 2012; 12(3 SUPPL.): 20–8.

Mysak J, Podzimek S, Sommerova P, Lyuya-Mi Y, Bartova J, Janatova T, Prochazkova J, Duskova J. Porphyromonas gingivalis: major periodontopathic pathogen overview. J Immunol Res. 2014; 2014: 1–8.

Liu J, Tang X, Li C, Pan C, Li Q, Geng F, Pan Y. Porphyromonas gingivalis promotes the cell cycle and inflammatory cytokine production in periodontal ligament fibroblasts. Arch Oral Biol. 2015; 60(8): 1153–61.

Enersen M, Nakano K, Amano A. Porphyromonas gingivalis fimbriae. J Oral Microbiol. 2013; 5: 1–10.

Dawes C, Pedersen AML, Villa A, Ekström J, Proctor GB, Vissink A, Aframian D, McGowan R, Aliko A, Narayana N, Sia YW, Joshi RK, Jensen SB, Kerr AR, Wolff A. The functions of human saliva: a review sponsored by the world workshop on oral medicine VI. Arch Oral Biol. 2015; 60(6): 863–74.

Kawas S Al, Rahim ZHA, Ferguson DB. Potential uses of human salivary protein and peptide analysis in the diagnosis of disease. Arch Oral Biol. 2012; 57: 1–9.

Frenkel ES, Ribbeck K. Salivary mucins in host defense and disease prevention. J Oral Microbiol. 2015; 7: 1–9.

Hannig C, Hannig M, Kensche A, Carpenter G. The mucosal pellicle – an underestimated factor in oral physiology. Arch Oral Biol. 2017; 80: 144–52.

Gabryel-Porowska H, Gornowicz A, Bielawska A, Wójcicka A, Maciorkowska E, Grabowska SZ, Bielawski K. Mucin levels in saliva of adolescents with dental caries. Med Sci Monit. 2014; 20: 72–7.

Corfield AP. Mucins: a biologically relevant glycan barrier in mucosal protection. Biochim Biophys Acta. 2015; 1850: 236–52.

Nakamura-Kiyama M, Ono K, Masuda W, Hitomi S, Matsuo K, Usui M, Nakashima K, Yokota M, Inenaga K. Changes of salivary functions in experimental periodontitis model rats. Arch Oral Biol. 2014; 59(2): 125–32.

Li X, Wang L, Nunes DP, Troxler RF, Offner GD. Pro-inflammatory cytokines expression in oral epithelial cells. J Dent Res. 2003; 82(11): 883–7.

Slomiany BL, Slomiany A. Porphyromonas gingivalis lipopolysaccharide-induced cytosolic phospholipase A2 activation interferes with salivary mucin synthesis via platelet activating factor generation. Inflammopharmacology. 2006; 14(3–4): 144–9.

Kusumawardani B, Soesatyo MH, Dasuki D, Asmara W. Maternal endotoxin-induced fetal growth restriction in rats: Fetal responses in toll-like receptor. Dent J (Maj Ked Gigi). 2012; 45(3): 144.

Huang S, Lu F, Zhang Z, Yang X, Chen Y. The role of psychologic stress-induced hypoxia-inducible factor-1α in rat experimental periodontitis. J Periodontol. 2011; 82(6): 934–41.

Cao X, Liu X, Hao Z, Ma C, Mao Z. Establishment of rat submandibular gland squamous cell carcinoma induced by DMBA. Hua xi kou qiang yi xue za zhi =. 2000; 18(3): 156–8.

Nonose R, Spadari APP, Priolli DG, Máximo FR, Pereira JA, Martinez CAR. Tissue quantification of neutral and acid mucins in the mucosa of the colon with and without fecal stream in rats. Acta Cir Bras. 2009; 24(4): 267–75.

Noguchi S, Ukai T, Kuramoto A, Yoshinaga Y, Nakamura H, Takamori Y, Yamashita Y, Hara Y. The histopathological comparison on the destruction of the periodontal tissue between normal junctional epithelium and long junctional epithelium. J Periodontal Res. 2017; 52: 74–82.

Mohamed A. The effect of diabetes mellitus on the thickness of gingival junctional epithelium. Thesis. Yogyakarta: Universitas Gadjah Mada; 2011. p. 1-72.

Bosshardt DD, Lang NP. The junctional epithelium: from health to disease. J Dent Res. 2005; 84: 9–20.

Brant JMC, Vasconcelos AC, Rodrigues L V. Role of apoptosis in erosive and reticular oral lichen planus exhibiting variable epithelial thickness. Braz Dent J. 2008; 19(3): 179–85.

Lombaert IMA, Brunsting JF, Weirenga PK, Faber H, Stokman MA, Kok T, Visser WH, Kampinga HH, de Haan G, Coppes RP. Rescue of salivary gland function after stem cell transplantation in irradiated glands. PLoS One. 2008; 3(4): 1–13.

Dhanisha SS, Guruvayoorappan C, Drishya S, Abeesh P. Mucins: structural diversity, biosynthesis, its role in pathogenesis and as possible therapeutic targets. Crit Rev Oncol Hematol. 2018; 122: 98–122.

Acquier AB, Busch L, Pita AKDC, Sanchez GA. Comparison of salivary levels of mucin and amylase and their relation with clinical parameters obtained from patients with aggressive and chronic periodontal disease. J Appl Oral Sci. 2015; 23(3): 288–94.

Proctor GB, Carpenter GH. Regulation of salivary gland function by autonomic nerves. Auton Neurosci Basic Clin. 2007; 133: 3–18.

Busch L, Borda E. Signaling pathways involved in pilocarpine-induced mucin secretion in rat submandibular glands. Life Sci. 2007; 80(9): 842–51.

Morris KE, St. Laurent CD, Hoeve RS, Forsythe P, Suresh MR, Mathison RD, Befus AD. Autonomic nervous system regulates secretion of anti-inflammatory prohormone SMR1 from rat salivary glands. Am J Physiol Cell Physiol. 2008; 296(3): C514–24.

Correia PN, Carpenter GH, Paterson KL, Proctor GB. Inducible nitric oxide synthase increases secretion from inflamed salivary glands. Rheumatology. 2010; 49: 48–56.


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