Free Radicals in the Oral Cavity

Free radicals are molecules with an unpaired electron. In a process called oxidation, an unpaired electron steals electrons from other molecules, creating new unstable free radicals. Free radicals occur naturally in the body but can be increased by environmental and lifestyle factors, such as nicotine, alcohol, or even dental procedures and materials such as bleaching agents, dental cements and composite fillings. Antioxidants are molecules that bond with the unpaired electron, neutralizing the oxidation.

What is a free radical?

Free radicals are molecules with an odd number of electrons, or better stated, with an unpaired electron. Since electrons normally exist in pairs, a molecule with an unpaired electron is unstable and it seeks a partner electron from another molecule. When the unpaired electron in the free radical molecule finds another molecule, it may steal an electron to complete its pair. This leaves the second molecule with an unpaired electron, that is, as a new free radical. This stealing process or electron theft -- what is known as oxidation -- can become a chain reaction.

What causes free radicals?

Some free radical molecules occur naturally in the body. They can be generated as part of metabolism as food is converted to energy in a gradual form of oxidation. The process releases individual electrons, leaving free-radical molecules. The new free radicals are chemically reactive and highly unstable. Free radicals can also be generated by other substances or activities within the body. For example, nicotine, alcohol, or dental procedures can raise the level of free radicals, especially within the oral cavity. Some molecules are more vulnerable to oxidation (i.e., electron theft) than others. In particular, some of the molecules in cell walls, containing unsaturated lipids, are particularly susceptible to the attack of free radicals. Other vulnerable molecules include RNA, DNA, and protein enzymes.

Why are free radicals a special problem for oral tissues?

Oral cells are uniquely susceptible to free radical damage because the mucus membranes allow rapid absorption of substances across their surfaces. This activity can be used for beneficial purposes, for example nitroglycerin tablets are placed under the tongue for rapid absorption to treat angina (chest pain). Direct exposure to noxious substances in the mouth further exacerbates the problem. Alcohol, nicotine from tobacco products, and dental materials such as hydrogen peroxide for bleaching, dental cements, composite fillings, and dental implants all increase free radicals and resulting cell damage.

Dental procedures and materials can increase free radicals?

The substances used in aesthetic procedures, such as bleaching or other whitening agents, can cause a dramatic increase in the level of free radicals in oral tissues. Dental implants, fillings and some dental materials, such as dental cements, composite fillings, all contribute to excess free radicals which may lead to oxidative stress.

Antioxidants: the antidote to free radicals

Fortunately, there are molecules that can safely interact with free radicals and terminate the chain reaction before vital cell molecules are damaged. These molecules are called antioxidants because they counteract the process of oxidation. The large, complex antioxidant molecules can bond with the unpaired electrons of free radicals, effectively neutralizing them. Different antioxidants work in different ways to either stop or retard the chain-reaction process of oxidation.

 

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  • An introduction to free radical biochemistry

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  • Cytotoxicity evaluation of Activ GP and Resilon sealers in vitro

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    Adverse tissue reactions of the gingiva and the periodontium - such as enhanced gingivitis and periodontitis - close to dental cast alloys may be caused by the effects of released metal elements. Tissue reactions depend upon the amounts of elements available which are a function of corrosion rates.

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    Patients with periodontal disease display increased bacterial antigen PMN number and activity; this proliferation results in high degree of free radical release culminating in heightened oxidative damage to gingival tissues, periodontal ligament and alveolar bone. Damage mediated by free radicals can be mitigated by “ANTIOXIDANT DEFENSE SYSTEM “. Physiological alteration and pathological states produced by free radicals depend on disequilibrium between free...

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  • N-Acetyl cysteine restores viability and function of rat odontoblast-like cells impaired by polymethylmethacrylate dental resin extract

    There is concern that dental-resin materials directly loaded on a prepared tooth adversely affect dental pulp tissue by releasing the resin chemicals through dentinal tubes. This study determined whether self-curing polymethyl methacrylate (PMMA)-based dental resin extract adversely affected the viability and function of odontoblast-like cells and whether the cytotoxicity of this resin, if any, could be eliminated by N-acetyl cysteine, an antioxidant...

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    This study was designed to evaluate the cytotoxicity of several resin-based cements (Panavia F, Super-Bond C&B, Chemiace II) after polymerization on cultured human dental pulp cells. After polymerization, three resin-based cements (Panavia F, Super-Bond C&B, Chemiace II) induced slight cytotoxicity. The sensitivity of cytotoxicity to human pulp cells depended on the resin-based cements and the concentration of the elution. Super-Bond C&B is the...

  • In vitro comparison of the cytotoxicity of acetal resin, heat-polymerized resin, and auto-polymerized resin as denture base materials

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  • The influence of various light curing units on the cytotoxicity of dental adhesives

    The objective of this study was to test the hypothesis that various light curing units (LCUs) have an influence on the cytotoxic action of adhesive systems. Significance: In practice, one should use combinations of dental adhesive and LCU in which the material has the least toxic influences.

  • Cytotoxicity of Titanium and Titanium Alloying Elements

    It is commonly accepted that titanium and the titanium alloying elements of tantalum, niobium, zirconium, molybdenum, tin, and silicon are biocompatible. However, research in the development of new titanium alloys for biomedical applications indicated that some titanium alloys containing molybdenum, niobium, and silicon produced by powder metallurgy show a certain degree of cytotoxicity. This group hypothesized that the cytotoxicity is linked to...

  • Mechanical properties and cytotoxicity of experimental soft lining materials based on urethane acrylate oligomers

    The purpose of this investigation was to determine whether experimental light-curing soft lining materials (ESLMs) based on commercially available urethane acrylate oligomers (UA-160TM, UV-3200B, UV-3500BA, and UV-3700B) are suitable for clinical use by measuring their viscosity, compressive modulus, Shore A hardness, tensile strength, adhesive strength, and cytotoxicity. The viscosities of the four ESLMs at 25 degrees C were 10.5 Pa.s, UV-3500BA; 144.0...

  • Real-time xCELLigence impedance analysis of the cytotoxicity of dental composite components on human gingival fibroblasts

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    Urethane dimethacrylate (UDMA) is used in dental restorative materials in its polymeric form. However, the process of polymerization is usually incomplete and the monomers of UDMA can diffuse into the oral cavity and the pulp, reaching millimolar concentrations. In the present work we showed that UDMA at 0.1 and 1.0 mM decreased the viability of and induced DNA damage in lymphocytes in...

  • Effects of Ethanol Consumption on Periodontal Inflammation in Rats

    Studies suggest a correlation between ethanol consumption and periodontal disease. We hypothesized that elevated levels of blood reactive oxygen species following ethanol consumption may increase inflammation in periodontal tissue. Results suggest that chronic alcohol consumption increased periodontal inflammation, oxidative damage, and TNF-? production and had an additive effect on polymorphonuclear leukocyte infiltration and gingival oxidative damage, increasing the severity of periodontal inflammation...  

  • The effect of BisGMA on cyclooxygenase-2 expression, PGE2 production and cytotoxicity via reactive oxygen species- and MEK/ERK-dependent and -independent pathways

    BisGMA released from composite resin may potentially affect the vitality of dental pulp and induce pulpal inflammation via stimulation of ROS production, MEK/ERK1/2 activation and subsequent COX-2 gene expression and PGE(2) production. Cytotoxicity of BisGMA to dental pulp cells is related to ROS production.

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    The substances used in aesthetic procedures, such as bleaching or other whitening agents, can cause a dramatic increase in the level of free radicals in oral tissues...

  • Effect of pH on element release from dental casting alloys

    Transient exposure of casting alloys to an acidic oral environment is likely to significantly increase elemental release from Ni-based alloys, but not from high-noble or noble alloys. Elemental release is important because it plays a significant role in alloy biocompatibility.

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    The results suggest that inflammatory stress and hyperglycemia may increase the corrosion of dental endosseous titanium-based implants, but that longer, more aggressive electrochemical conditions may be necessary to fully assess these effects.

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    Under the conditions of this study, toothbrushing increased the elemental release from dental casting alloys...

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    Brushing dental casting alloys may increase their cytotoxicity in vitro, but the increase depends heavily on the alloy type and brushing condition...