ANOMALY PROTEIN OF ORAL MUCOSAL INDUCES RECURRENT APHTHOUS ULCERATION

Diah Savitri Nugroho

Abstract


Recurrent Aphthous Ulceration (RAU) is a type of local inflammation of the oral mucosa with symptomatic soft tissue damage. The prevalence of RAU is about 17-67%. Dominant factors causing this disease are understood, but there are predicted internal and external factors that cause related immune disorders. RAU is initiated by mucous proteins which continuously stimulate a physiological response required for a pathophysiological reaction. The aim of this study was to characterize specific anomaly proteins in oral mucosa as causing the initiation of RAU. Samples of mucosal proteins from 30 RAU patients were analyzed with sodium dodexylsulphate polyacrylamid gelelectrophorese (SDS-PAGE) and visualized with silver stain (AgNO3) showing proteins with a range of molecular weight 27 – 180 kDa. Western blotting using a polyclonal antibody specific to RAU showed that the specific proteins of RAU have molecular weights of 23, 27, 65, 70 and 87 kDa. The finding of so many proteins appears to be a new phenomenon, suggesting that the initiation of RAU is possibly due to a continuous induction of internal and external reactions by several mucosal proteins, that become anomaly proteins of high reactivity and antigenicity. This situation can cause overreaction on the oral mucosa with specific symptoms that are known as a RAU.

 


Full Text: PDF

Refbacks

  • There are currently no refbacks.


Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.

Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.
<a target="_new" rel="license" href="http://creativecommons.org/licenses/by/3.0/">
			<img alt="Creative Commons License" style="border-width:0" src="http://i.creativecommons.org/l/by/3.0/80x15.png"/>
		</a>
		<br/>
		This work is licensed under a <a rel="license" target="_new" href="http://creativecommons.org/licenses/by/3.0/">Creative Commons Attribution 3.0  License</a>.