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Table of Contents
Year : 2022  |  Volume : 9  |  Issue : 1  |  Page : 14-17

Anticaries vaccine

1 Assistant Professor, Department of Conservative and Endodontics, Government College of Dentistry, Indore, India
2 Assistant Professor, Department of Periodontia, Government College of Dentistry, Indore, India
3 Reader, Department of Conservative Dentistry and Endodontics, RKDF Dental College and Research Centre, Bhopal, India
4 Professor, Department of Conservative Dentistry and Endodontics, Index Institute of Dental Sciences, Indore, India
5 Tutor, Department of Conservative and Endodontics, Government College of Dentistry, Indore, India
6 Private Practioner, Surat, India

Date of Submission21-Feb-2022
Date of Acceptance03-Mar-2022
Date of Web Publication24-Mar-2022

Correspondence Address:
Dr. Neelam Vijaywargiya
Department of Conservative and Endodontics, Government College of Dentistry, Indore, Madhya Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpcdr.ijpcdr_3_22

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The mutans streptococci bacteria have long been acknowledged as the prime disease-instigating agents in dental caries, the disease that causes tooth decay. Caries vaccines have shown promising outcomes in animal trials, but they are still far from being effective in humans owing to political, monetary, as well as ethical concerns. Candidate vaccines must be evaluated in clinical trials to progress toward practical vaccine development. Passive immunization strategies that appear to be promising will need to be tested further in the clinic.

Keywords: Anticaries vaccine, dental caries, Streptococcus mutans

How to cite this article:
Vijaywargiya N, Verma M, Saxena D, Ganguly S, Pagare N, Khatri M. Anticaries vaccine. Int J Prev Clin Dent Res 2022;9:14-7

How to cite this URL:
Vijaywargiya N, Verma M, Saxena D, Ganguly S, Pagare N, Khatri M. Anticaries vaccine. Int J Prev Clin Dent Res [serial online] 2022 [cited 2023 Jun 10];9:14-7. Available from: https://www.ijpcdr.org/text.asp?2022/9/1/14/340842

  Introduction Top

Dental caries is the second-most common disease in humans, after the common cold. Conferring to the WHO, caries is defined as “localized posteruptive, a pathological process of external origin involving softening of hard-tooth tissue and proceeding to the formation of a cavity.” Several caries aversion stratagems are currently in practice, including oral health education, chemical, mechanical plaque control, pit, fissure sealants, fluoride use, and so on. Many of these strategies have the potential to be successful. However, economic, behavioral, and cultural blockades to their usage have contributed to the global epidemic of children's dental disease.[1],[2] The utmost current strategy for combating dental caries is to develop an effectual vaccine that will be well-suited for public health usage, particularly in environments where regular oral health care is difficult to come by.

  Vaccines Top

Vaccines are immunobiological substances that provide a targeted shield in contrast to a specific disease. It boosts the release of a defensive antibody as well as other immune reactions. Live modified organisms, inactivated or killed organisms, extracted cellular fractions, toxoids, or a blend of these are used to make vaccines.[3]

  Mechanism of Action of Vaccine Top

Saliva comprises about 1%–3% immunoglobulin, most of which are secretaries of IgA. Nevertheless, saliva as well comprises humoral immunoglobulin IgG as well as IgM from gingival sulcular fluid. In addition, parts of immune cells, for instance, lymphocytes, macrophages, as well as neutrophils, are also present in the gingival sulcus. Salivary immunoglobulin might work as a specific agglutinin that binds to bacterial surface receptors in addition also averts colonization along with subsequent caries formation. They can also deactivate surface glucosyltransferase (GTF), that might decrease the accumulation of extracellular glucans leading to a decline in plaque formation.[4],[5] Salix cells produce secretory IgA antibodies by Gut-Associated Lymphoid Tissue (GALT) since B is sensitive. Cells may be home to salivary glands. IgA antibodies are salivary glands with straight admittance to the dental area. They may avert Streptococcus mutans in adhesion to its enamel or may inhibit dextran formation by inhibiting GTF activity.[6] Gingival crevicular mechanism comprises all parts of the humoral and connective tissue, that might perform its function in the tooth area. There is now enough testimony to explain the potential after subcutaneous S. mutans vaccination. Organism is phagocytosed then endures antigenic processing by macrophages. In lymphoid tissue, T as well as B-lymphocytes are sensitive to macrophages that inhibit. The human leukocyte antigen. Class-II antigen complex besides which it releases interleukin (IL)-I. This triggers the CD-4 as well as CD-8 cytotoxic suppressor cell reaction by activating IL-2 receptors and releasing IL2. Interactions amid cells play an important role in regulating the release of IgG, IgA, as well as IgM antibodies along with B-lymphocytes.[7],[8],[9]

  Trials Top

Animal trials

In most immunization trials, rats and monkeys have been used. Rodents are a good choice for laboratory animals because they can make a correct diagnosis of caries by examining the tooth surface and establishing large experimental groups. Mutant streptococci (MS) have been shown in numerous trials to cause caries in pits and fissures, in addition to on the smooth, approximal, as well as root surfaces of the teeth of both gnotobiotic along with conventional animals. Immunization trials have provided more testimony for MS involvement in the etiology of caries. In one trial, oral administration of S. mutans cells to gnotobiotic rats resulted in the release of secretory antibodies in the saliva, which was linked to a decline in the incidence of caries in these animals. Tonsillar usage of formalin-killed Streptococcus sobrinus cells to rabbits reduced caries areas to one-fifth of those in nonimmune rabbits.[10]

Human trials

Because dental caries meets the norms for an infectious disease, researchers have looked into the prospect of averting it through vaccination. The theory is that immunizing against S. mutans will trigger an immune reaction, averting the organism from colonizing the tooth surface and averting decay. Because the vaccine would be given prior to deciduous dentition erupting at around 6 months of age, it would protect children who have the highest rate of caries. The vaccine can be given simultaneously with diphtheria as well as tetanus vaccines. Immunity could then be boosted at regular intervals for lifelong protection. The prevailing immunization delivery system could be utilized shorn of incurring any monetary costs.[4] Clinical trials are currently underway to see if a S. mutans pill can help avert caries. Human trials have yielded some contradictory outcomes so far. Some researchers have discovered a link between secretory-IgA and the prevalence of caries. This outcome, however, may perhaps be due to the experimental design. Ingestion of capsules containing S. mutans has been shown to stimulate the release of secretory-IgA. In humans, serum immunoglobulin stimulation has yielded mixed outcomes, besides no link could be found amid caries as well as serum immunoglobulin stimulation.[11],[12]

  Routes of Administration of Vaccine Top

Two important ways to manage the common mucosal immune pathway are:-

  1. Systemic route
  2. Active gingiva-salivary route.

The induction of secretory IgA antibodies is best accomplished through the use of the common mucosal immune system. The following techniques are employed:

Oral induction of immunity

In the GALT, oral induction of immunity was used. Antigen is best applied through oral feeding, gastric intubation, or vaccines comprising capsules or liposomes.

To avoid colonization and aggregation of microorganisms, the Nasopharynx - associated lymphoid tissue (NALT) nasal route administration protocol is favored to persuade immunity to bacterial antigens.

Minor salivary gland

One of the best routes is because it takes less time besides having broad ducts that allow bacteria and their products to pass backward.


A trial found that giving formalin-killed S. sobrinus cells to rabbits via tonsillar administration reduced the number of various sites. IgA antibodies can be produced in both the major as well as minor salivary glands subsequent to repeated usage.[13],[14],[15],[16]


As a consequence of the high concentration of lymphoid follicles in the lower intestinal tract, it is known as an inductive location for immune reactions.

Systemic route

Antibodies IgG, IgM, and IgA enter the oral cavity via glucosyltransferase (GCF) in addition to protect against dental caries. However, increased serum IgG antibodies were found to be the most important factor in caries protection.

The active gingiva-salivary route is considered the best route for immunity induction because it has fewer side effects. This method can produce both IgA and IgG antibodies.[9]

Immunization by passive means

  1. Monoclonal antibodies have been tested against the cell surface Ag I/II of S. mutans. S. mutans were observed to be more pretentious besides exhibited massive decline in numbers in a topical usage where there were more of them
  2. Bovine milk: Polyclonal IgG antibodies have been found in bovine milk and whey after cows were given a vaccine containing whole S. mutans. A rat model's diet was then supplemented with this. Caries levels decreased as a result of the immune whey[17]
  3. Antibodies to egg yolk: The occurrence of formalin-killed whole cells as well as cell-associated GTFs resulted in a decline in caries
  4. Transgenic plants: This is the first genetically modified plant-based vaccine. Because it is tasteless in addition to being colorless, it can be utilized directly to the teeth.[18]

  The Consequences of Getting A Caries Vaccine Top

Even when made and used properly, all vaccines appear to be harmful. Sera from other rheumatic fever patients exhibit serological cross-reactivity amid cardiac antigen in addition to certain antigens from hemolytic Streptococci, which are very dangerous.[19] Antiserum from rabbits vaccinated by St. John's wort cells. Mutans perfect and S. mutans high-molecular-weight protein antigen were found to be shared with normal rabbits and human heart tissue in a test. Streptococcus cells of S. mutans and Streptococcus ratti contain polypeptides (62–67 KDA) that respond negatively to human heart tissue and myosin rabbit skeletal muscle.[20] Exhibits, in contrast, reveal that the rabbit antiserum to Todd-Hewitt is a broth of parts of the weight of the upper cells that respond to the monkey heart muscle in S. mutans combined with intermediate parts. Rhesus monkeys and rabbits vaccinated with purified Ag I/II from S. mutans do not make antibodies that work in the heart. Increased release of cardiac antibodies in rabbits vaccinated against MS leads to damage to the heart muscle due to binding to Streptococcal polypeptide. The development of a vaccine under the tooth decay control unit has aroused the interest of researchers due to the ability of complete Streptococcal cells to target active cardiovascular antibodies. Cross-reactivity of GTF containing human heart tissue was also tested, but the outcomes were negative.[7] Supplementary research reveals that the C-terminal Ag I/II contains epitope that shares human IgG. In addition, even though the clinical significance of these findings is unknown, it gives the impression that this potentially harmful epitope should be avoided with the caries vaccine. Some MS, for example, S. sobrinus, in addition to nonmutans streptococci, have an active IgG component.[21]

  Conclusions Top

Many questions must be answered before a dental caries vaccine can be acknowledged by the dental profession. One crucial question is what effect shifting the indigenous oral microflora will have in the long run. Furthermore, can the pathogen, S. mutans, be immunologically inactivated at the highest level of caries activity? Immunization can control which S. mutans entry pathways into the dental biofilm. Can virulence factors allied with S. mutans trigger an immune reaction? In comparison to other caries aversion methods, how safe is the dental caries vaccine? Given the decline in caries prevalence over the past several decades, will the profession accept vaccination as a caries aversion mechanism? Despite the fact that scientific, regulatory, and economic obstacles must be overcome to achieve this goal, the potential benefit continues to make the race worthwhile.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Shivakumar KM, Vidya SK, Chandu GN. Dental caries vaccine. Indian J Dent Res 2009;20:99-106.  Back to cited text no. 1
[PUBMED]  [Full text]  
Fukuizumi T, Inoue H, Tsujisawa T, Uchiyama C. Tonsillar usage of formalin-killed cells of Streptococcus sobrinus reduces experimental dental caries in rabbits. Infect Immun 1999;67:426-8.  Back to cited text no. 2
Childers NK, Tong G, Li F, Dasanayake AP, Kirk K, Michalek SM. Humans immunized with Streptococcus mutans antigens by mucosal routes. J Dent Res 2002;81:48-52.  Back to cited text no. 3
Iwaki M, Okahashi N, Takahashi I, Kanamoto T, Sugita-Konishi Y, Aibara K, et al. Oral immunization with recombinant Streptococcus lactis carrying the Streptococcus mutans surface protein antigen gene. Infect Immun 1990;58:2929-34.  Back to cited text no. 4
Lehner T. Immunology of dental caries. In: Immunology of Oral Diseases. 3rd ed. United States: Blackwell Scientific Publications; 1992.  Back to cited text no. 5
Bowen WH, Cohen B, Cole M, Colman G. Immunization against dental caries: Summary. J Dent Res 1976;55:65-68.  Back to cited text no. 6
Katz J, Harmon CC, Buckner GP, Richardson GJ, Russell MW, Michalek SM. Protective salivary immunoglobulin A responses against Streptococcus mutans infection after intranasal immunization with S. mutans antigen I/II coupled to the B subunit of cholera toxin. Infect Immun 1993;61:1964-71.  Back to cited text no. 7
Wilton JM. Future control of dental disease by immunization: Vaccines and oral health. Int Dent J 1984;34:177-83.  Back to cited text no. 8
Russell RR, Johnson NW. The prospects for vaccination against dental caries. Br Dent J 1987;162:29-34.  Back to cited text no. 9
Lehner T. Future possibilities for the prevention of caries and periodontal disease. Br Dent J 1980;149:318-25.  Back to cited text no. 10
Bowen WH. Do we need to be concerned about dental caries in the coming millennium? Crit Rev Oral Biol Med 2002;13:126-31.  Back to cited text no. 11
Russell RR, Beighton D, Cohen B. Immunisation of monkeys (Macaca fascicularis) with antigens purified from Streptococcus mutans. Br Dent J 1982;152:81-4.  Back to cited text no. 12
Koga T, Oho T, Shimazaki Y, Nakano Y. Immunization against dental caries. Vaccine 2002;20:2027-44.  Back to cited text no. 13
Smith DJ. Dental caries vaccines: Prospects and concerns. Crit Rev Oral Biol Med 2002;13:335-49.  Back to cited text no. 14
Moro I, Lehner T. Sixth International Congress of Mucosal Immunology, July 23, 1990. Dental caries vaccines. J Dent Res 1990;69:1863-4.  Back to cited text no. 15
Russell RR. The application of molecular genetics to the microbiology of dental caries. Caries Res 1994;28:69-82.  Back to cited text no. 16
Luo Z, Smith DJ, Taubman MA, King WF. Cross-sectional analysis of serum antibody to oral streptococcal antigens in children. J Dent Res 1988;67:554-60.  Back to cited text no. 17
Russell MW, Hajishengallis G, Childers NK, Michalek SM. Secretory immunity in defense against cariogenic mutans streptococci. Caries Res 1999;33:4-15.  Back to cited text no. 18
Smith DJ, Taubman MA. Oral immunization of humans with Streptococcus sobrinus glucosyltransferase. Infect Immun 1987;55:2562-9.  Back to cited text no. 19
Michalek SM, McGhee JR, Mestecky J, Arnold RR, Bozzo L. Ingestion of Streptococcus mutans induces secretory immunoglobulin A and caries immunity. Science 1976;192:1238-40.  Back to cited text no. 20
Brandtzaeg P. The B-cell development in tonsillar lymphoid follicles. Acta Otolaryngol Suppl 1996;523:55-9.  Back to cited text no. 21


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