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Enzymes, dentinogenesis and dental caries: a literature review.

Larmas M, Sándor GK - J Oral Maxillofac Res (2014)

Bottom Line: Alkaline phosphatase activity sharply decreased when odontoblasts turned into quiescent odontoblasts.Proteolytic activity was especially demonstrable using histochemical and biochemical means.Specifically, matrix metalloproteases may have originated partly from activated proenzymes of host origin.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pediatric Dentistry and Cariology, Institute of Dentistry, University of Oulu, Oulu Finland.

ABSTRACT

Objectives: Search in PubMed with keywords "enzymes, dentinogenesis, and dental caries" revealed only 4 items, but when combined with "enzymes, osteogenesis, and osteoporosis" as high as 404 items resulted. Dental caries was associated with an order of magnitude fewer studies than the chronic bone disease, osteoporosis. This observation motivated this review.

Material and methods: A comprehensive review of the available literature on role of enzymes in dentinogenesis and dental caries was undertaken using MEDLINE (PubMed) and Scopus. Keywords for the search were: enzymes and odontoblasts, enzymes and different forms of dentinogenesis as well as dental caries.

Results: Search revealed studies which described odontoblasts harbouring numerous enzymes (hydrolases, including metalloproteinases, transaminases and dehydrogenases) during primary dentinogenesis. Alkaline phosphatase activity sharply decreased when odontoblasts turned into quiescent odontoblasts. Tertiary dentinogenesis was characterized first by reactionary dentine formation when alkaline phosphatase was highly reactivated. Then later some of these odontoblasts may die out and be replaced by other progenitor cells of pulpal origin. This tertiary dentine was called reparative dentine. Pulpal progenitor/stem cells revealed alkaline phosphatase activity in areas encircling inflamed pulp sections. Soft carious dentine revealed high hydrolase, transaminase and dehyrogenase activities that may have originated from invading microbes, saliva or were endogenous. Proteolytic activity was especially demonstrable using histochemical and biochemical means. Specifically, matrix metalloproteases may have originated partly from activated proenzymes of host origin.

Conclusions: Though dental studies are scanty when compared to bone, the active role of large spectrum of enzymes in healthy and carious dentine was given support.

No MeSH data available.


Related in: MedlinePlus

A = A microradiograph of a developing human molar tooth with an advanced carious lesion. Undecalcified frozen section (10 micrometer thick) of an extracted human molar tooth. Original magnification x8. B = Localization of alkaline phosphatase activity in the odontoblasts, predentine, cementum, in remaining parts of the periodontal ligament, and some pulpal cells. Substrate: 1-naphthyl acid phosphate, Fast Blue RR, pH 9.2). Original magnification x6. C = Higher magnification of the localization of alkaline phosphatase activity in pulpal cells under the advanced carious lesion with pulp perforation and pulpal inflammation. Note the disappearance of enzyme activity in odontoblasts in the site of carious exposure and appearance in dentinal tubules in soft carious dentin. Original magnification x48. D = Higher magnification of the same area of pulp horn showing the presence of arylaminopeptidase activity in the fibroblasts/progenitor/stem cells or inflammatory cells in the inflamed pulp horn. Substrate: N-L-arginyl-2-naphthylamine, Fast Blue B, pH, 6.8. Original magnification x48. The picture is originally published in The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology, 296, p. 565, 2013, and the reproduction granted by WILEY/ the Copyright Clearence Center Inc, License Number 3213520064351.
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fig2: A = A microradiograph of a developing human molar tooth with an advanced carious lesion. Undecalcified frozen section (10 micrometer thick) of an extracted human molar tooth. Original magnification x8. B = Localization of alkaline phosphatase activity in the odontoblasts, predentine, cementum, in remaining parts of the periodontal ligament, and some pulpal cells. Substrate: 1-naphthyl acid phosphate, Fast Blue RR, pH 9.2). Original magnification x6. C = Higher magnification of the localization of alkaline phosphatase activity in pulpal cells under the advanced carious lesion with pulp perforation and pulpal inflammation. Note the disappearance of enzyme activity in odontoblasts in the site of carious exposure and appearance in dentinal tubules in soft carious dentin. Original magnification x48. D = Higher magnification of the same area of pulp horn showing the presence of arylaminopeptidase activity in the fibroblasts/progenitor/stem cells or inflammatory cells in the inflamed pulp horn. Substrate: N-L-arginyl-2-naphthylamine, Fast Blue B, pH, 6.8. Original magnification x48. The picture is originally published in The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology, 296, p. 565, 2013, and the reproduction granted by WILEY/ the Copyright Clearence Center Inc, License Number 3213520064351.

Mentions: When the carious process was so progressive that it reached the dental pulp in a developing human molar tooth, the histochemical distribution of APase was interesting: enzyme activity disappeared from the odontoblasts of the pulp exposure area, where cells evidently were not vital any more in these growing teeth [52]. All other odontoblasts around the pulp chamber exhibited strong APase activity, especially in the cells of the open root apices, but also periodontal structures on the root surface around the apex areas, exhibited high activity (Figure 2).


Enzymes, dentinogenesis and dental caries: a literature review.

Larmas M, Sándor GK - J Oral Maxillofac Res (2014)

A = A microradiograph of a developing human molar tooth with an advanced carious lesion. Undecalcified frozen section (10 micrometer thick) of an extracted human molar tooth. Original magnification x8. B = Localization of alkaline phosphatase activity in the odontoblasts, predentine, cementum, in remaining parts of the periodontal ligament, and some pulpal cells. Substrate: 1-naphthyl acid phosphate, Fast Blue RR, pH 9.2). Original magnification x6. C = Higher magnification of the localization of alkaline phosphatase activity in pulpal cells under the advanced carious lesion with pulp perforation and pulpal inflammation. Note the disappearance of enzyme activity in odontoblasts in the site of carious exposure and appearance in dentinal tubules in soft carious dentin. Original magnification x48. D = Higher magnification of the same area of pulp horn showing the presence of arylaminopeptidase activity in the fibroblasts/progenitor/stem cells or inflammatory cells in the inflamed pulp horn. Substrate: N-L-arginyl-2-naphthylamine, Fast Blue B, pH, 6.8. Original magnification x48. The picture is originally published in The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology, 296, p. 565, 2013, and the reproduction granted by WILEY/ the Copyright Clearence Center Inc, License Number 3213520064351.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4306321&req=5

fig2: A = A microradiograph of a developing human molar tooth with an advanced carious lesion. Undecalcified frozen section (10 micrometer thick) of an extracted human molar tooth. Original magnification x8. B = Localization of alkaline phosphatase activity in the odontoblasts, predentine, cementum, in remaining parts of the periodontal ligament, and some pulpal cells. Substrate: 1-naphthyl acid phosphate, Fast Blue RR, pH 9.2). Original magnification x6. C = Higher magnification of the localization of alkaline phosphatase activity in pulpal cells under the advanced carious lesion with pulp perforation and pulpal inflammation. Note the disappearance of enzyme activity in odontoblasts in the site of carious exposure and appearance in dentinal tubules in soft carious dentin. Original magnification x48. D = Higher magnification of the same area of pulp horn showing the presence of arylaminopeptidase activity in the fibroblasts/progenitor/stem cells or inflammatory cells in the inflamed pulp horn. Substrate: N-L-arginyl-2-naphthylamine, Fast Blue B, pH, 6.8. Original magnification x48. The picture is originally published in The Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology, 296, p. 565, 2013, and the reproduction granted by WILEY/ the Copyright Clearence Center Inc, License Number 3213520064351.
Mentions: When the carious process was so progressive that it reached the dental pulp in a developing human molar tooth, the histochemical distribution of APase was interesting: enzyme activity disappeared from the odontoblasts of the pulp exposure area, where cells evidently were not vital any more in these growing teeth [52]. All other odontoblasts around the pulp chamber exhibited strong APase activity, especially in the cells of the open root apices, but also periodontal structures on the root surface around the apex areas, exhibited high activity (Figure 2).

Bottom Line: Alkaline phosphatase activity sharply decreased when odontoblasts turned into quiescent odontoblasts.Proteolytic activity was especially demonstrable using histochemical and biochemical means.Specifically, matrix metalloproteases may have originated partly from activated proenzymes of host origin.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pediatric Dentistry and Cariology, Institute of Dentistry, University of Oulu, Oulu Finland.

ABSTRACT

Objectives: Search in PubMed with keywords "enzymes, dentinogenesis, and dental caries" revealed only 4 items, but when combined with "enzymes, osteogenesis, and osteoporosis" as high as 404 items resulted. Dental caries was associated with an order of magnitude fewer studies than the chronic bone disease, osteoporosis. This observation motivated this review.

Material and methods: A comprehensive review of the available literature on role of enzymes in dentinogenesis and dental caries was undertaken using MEDLINE (PubMed) and Scopus. Keywords for the search were: enzymes and odontoblasts, enzymes and different forms of dentinogenesis as well as dental caries.

Results: Search revealed studies which described odontoblasts harbouring numerous enzymes (hydrolases, including metalloproteinases, transaminases and dehydrogenases) during primary dentinogenesis. Alkaline phosphatase activity sharply decreased when odontoblasts turned into quiescent odontoblasts. Tertiary dentinogenesis was characterized first by reactionary dentine formation when alkaline phosphatase was highly reactivated. Then later some of these odontoblasts may die out and be replaced by other progenitor cells of pulpal origin. This tertiary dentine was called reparative dentine. Pulpal progenitor/stem cells revealed alkaline phosphatase activity in areas encircling inflamed pulp sections. Soft carious dentine revealed high hydrolase, transaminase and dehyrogenase activities that may have originated from invading microbes, saliva or were endogenous. Proteolytic activity was especially demonstrable using histochemical and biochemical means. Specifically, matrix metalloproteases may have originated partly from activated proenzymes of host origin.

Conclusions: Though dental studies are scanty when compared to bone, the active role of large spectrum of enzymes in healthy and carious dentine was given support.

No MeSH data available.


Related in: MedlinePlus