Dr John Gabrovsek

Received: January 1997


Dental Caries Part 1 Dental Caries Part 3 Dental Caries Part 4

Dental caries was rather common and increasing in European population in post World War II era. However, I remember very well studying in periodontology the case of Juvenile idiopathic periodontitis we named at that time "Juvenile periodontosis".The patient was a young man maybe twenty years old who had reabsorbed alveolar bone in incisor and molar region and his teeth were loose and movable, but he didn't have any carious lesion in his mouth. My teacher Prof. Brencic was together with Orban the student of Gotlieb in Vienna some time before WW II. According to Brencic, Gotlieb described many years earlier the observation that in Juvenile idiopathic periodontitis which he termed at that time "diffuse atrophy of the alveolar bone" patients have very few caries lesions or lacking dental caries completely. One can find the same observation described by Orban in American literature in 1950's and 1960's (Orban,1958)(Orban,1967). But in more recent times the lack of dental caries in Juvenile idiopathic periodontitis patients is not mentioned any more. Nevertheless, my own observation of patients with Juvenile idiopathic periodontitis that lack dental caries made a permanent impression on me.

In pathophysiology courses we also learned that the development of pathological processes particularly in the case of infection is characterized by two basic features: the activity of the agent, which is considered as causative, and the capability of the host to respond to the action of etiologic factors, called reactivity of the host. It was emphasized that the reactivity is the base for the pathogenesis of the disease.

It was obvious that I could not be convinced with the explanation of the development of dental caries by the proteolytic theory which was prominent at the time. The first reason was that the theory could not explain why Juvenile idiopathic periodontitis patients were lacking caries lesions while living among the population with numerous caries lesions. The second reason was that this theory did not implicate the host's responses (reactivity)to dental caries infection.

In the 1960's I learned that the acid decalcification theory regained again prominent status. The culmination in the argument against the proteolytic involvement in dental caries development has been an experiment in which monocontaminated animals with a non-gelatinase producing non-proteolytic alpha type of Streptococcus developed carious lesions (Orlando et al,1955). These results prompted Fitzgerald to comment: "Thus it may be that what has been termed proteolysis is unnecessary for the formation of dental caries" (Fitzgerald,RJ,1959). The above mentioned experiment in which monocontaminated animals with nonproteolytic alpha type of Streptococcus developed carious lesion prove only that the source of the enzymes could not be from the bacteria.

Why do researchers not even consider that the host could be the source of enzymes which brake down the organic component of the enamel and dentin in caries development? I would like to know the reason.

The acid decalcification theory did not convince me for exactly the same reason that the proteolytic theory did not. It is a proven fact that mucosa is the source of neutrophil leucocytes entering into the oral cavity. These cells are rich in lysosomes loaded with the enzymes which brake down sugars, fats, and proteins. Most of these enzymes are active only in an acidic environment.That is why these enzymes are also called acid hydrolyses (they were discovered by DeDuve). It was mentioned in part one that leucocytes release lysosomal enzymes into the extracellular environment when the most cariogenic conditions exist, that is in presence of Streptococcus mutans and sucrose (Baehni et al,1977).

What is the role of lysosomal enzymes in dental caries development?

The following clinical cases need consideration and more attention from the cariologists:

  1. Juvenile Idiopathic Periodontitis, which I already mentioned.
  2. Down's Syndrome
  3. IgA Immunodeficiency

Down's Syndrome is a special case as far as dental caries is concerned. One would expect that these patients would develope more carious lesions than normal controls. But numerous studies indicate otherwise. There is some criticism of institutional studies that may not be accurate because of lack of normal controls. But studies of families with children with Down's syndrome and comparing them with their normal siblings do not have such a deficiency. I am quoting Orner:"The dental caries experience of a sample of 212 children with Down's syndrome was contrasted with that of 124 of their unaffected sibs. The affected children had caries experience less than one-third of the sibs. The experience of the sibs however was not different from that of other normal children . This differential caries experience could not be explained by differences between groups in their exposure to risk of the disease" (Orner,G, 1975).

The role of salivary sIgA in protection against dental caries development is still a matter of debate. The correlation between sIgA levels and caries development has been studied with conflicting results. However, the number of papers is growing, which report that immunoglobulin content in the saliva increases in case of high caries experience (Weyna et al,1979)(Hocini et al,1993) (Parkash et al,1994) (Dens et al,1995).

On the other hand Robertson's group studied pair-matched patients with IgA deficiency and immunocompetent subjects by age and plaque index. During a two years period they observed less caries experience in immunodeficient patients than in normal controls (Robertson et al,1980) Fernandes and his collaborators also observed that IgA-deficient children showed caries scores lower than those of healthy children (Fernandes et al,1995)

I discovered that Juvenile idiopathic periodontitis patients, Down's syndrome patients, and IgA immunodeficient patients have two things in common.They were found to have significantly less caries compared to normal control groups, and all three groups are associated with defective leucocytes (PMNs) chemotaxis (Khan et al, 1975) (Lavine et al, 1979)(D'Amelio at al, 1980)

The above described observations contrast with the traditional view which considers environmental factors mainly in dental caries development. The described evidence however does not negate environmental factors but rather compliments them with the host's response.

Traditionally leucocytes response in the oral cavity to dental caries infection is ignored as if does not exist. The host's leucocytes derived enzymes (acid hydrolases) certainly contribute in part to dental caries development.


D'Amelio, R, LeMoli, S, Rossi, P, Aiuti, F. (1980) Neutrophil Chemotaxis Defect in IgA Deficiency Evalated by Migration Agarose Method. Scand. J. Immunol. 11, 471-477.

Dens,F, Boute,P, Vinckier,F, Declerck,D.(1995) Quantitative Determination of Immunologic Components of Salivary Gland Seccretion in Long-term, Event-free Pediatric Oncology Patients. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, & Enndodontics. 79(6), 701-704.

Fernandes, FR, Nagao, AT, Mayer, MP, Zelante, F, Carneiro-Sampaio, MM.(1995) Compensatory Levels of Salivary IgM Anti-Streptococcus Mutans Antibodies in IgA-deficient Patients.Journal of Investigational Allergology & Clinical Immunology.5(3),151-155.

Fitzgerald,RJ.(1959) in Orland, FJ. A Review of Dental Research Using Germfree Animals. Ann. N.Y. Acad.Sci.78, 285-289.

Hocini,H, Iscaki,S, Bouvet,JP, Pillot,J.(1993) Unexpectedly High Levels of Some Presumably Protective Secretory Immunoglobulin A Antibodies to Dental Plaque Bacteria in Salivas of both Caries- Resistant and Caries-Susceptible Subjects. Infection & Immunity 61, (9),3597-3604.

Khan,AJ, Evans,HE, Glass,L, Shin,YH, Almonte,D.(1975) Defective Neutrophil Chemotaxis in Patients with Down Syndrome. The Journal of Pediatrics. 87,87-89.

Lavine,WS, Maderazo,EG, Stolman,J, Ward, PA, Cogen,RB, GreenblattI, Robertson,PB.(1979) Impaired Neutrophil Chemotaxis in Patients with Juvenile and Rapidly Progressing Periodontitis. J. Periodont. Res.14, 10-19.

Orban,B. (1958) Periodontics. The C.V. Mosby Company Saint Louis. 331.

Orban,B. (1967) Clasification and Nomenclature of Periodontal Diseases. in Lazare,A ed. Periodontal Therapy: A Review. New York. New York University Press . London. University of London Press Limited

Orland,FJ. Blayney,JR, Harrison,RW, Reyniers,JA, Trexler,PC, Ervin, RF, Gordon,HA, Wagner,M.(1955) Experimental Caries in Germ-free Rats Inoculated with Enterococci. J.Am.Dent.Assoc. 50, 259-272.

Orner,G.(1975) Dental Caries Experience Among Children with Down's Syndrme and Their Sibs. Arch.Oral.Biol. 20,627-634.

Parkash,H, Sharma,A, Banerjee,U, Sidhu,SS, Sundaram,KR.(1994) Humoral Immune Response to Mutans Streptococci Associated with Dental Caries. National Medical Journal of India. 7(6),263-266.

Robertson,PB, Mackler,BF, Wright,TE, Levy,BM.(1980) Periodontal Status of Patients With Abnormalities of the Immune System. J.Periodontol. 51,70-73.

Weyna,E, Jaworska,D, Dabrowski,W, Strzelecka,G.(1979) Dental Caries, Periodontal Disease and Salivary Immunoglobulins. Stomatologie der DDR. 29(5),353-356.


Return to Dentistry On-Line Professional Contents

All pages copyright Priory Lodge Education Ltd 1994 - 1997.