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Year : 2020 | Volume
: 31
| Issue : 5 | Page : 782-783 |
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Hard tissue formation in odontogenic lesions associated with impacted tooth: Plausible pathogenesis |
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Arush Thakur1, Pooja Siwach2, Ruchika R Agrawal1
1 Department of Oral Pathology and Microbiology, Government Dental College and Hospital, Mumbai, Maharashtra, India 2 Department of Dentistry, Government Medical College and General Hospital, Dhule, Maharashtra, India
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Date of Submission | 30-Nov-2018 |
Date of Decision | 13-Feb-2020 |
Date of Acceptance | 06-Mar-2020 |
Date of Web Publication | 08-Jan-2021 |
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Abstract | | |
Odontogenesis is a complex process, which involves the molecular interaction between the epithelium and ectomesenchyme called as epithelium mesenchymal interaction (EMI). Reduced enamel epithelium (REE) after tooth formation protects enamel from coming in contact with adjacent ectomesenchyme. Also, REE acts as a source of origin for odontogenic lesions, during the process of development of a lesion, disruption in REE may occur and lead to formed enamel coming in contact with adjacent ectomesenchyme leading to the formation of cementum like calcifications. REE may play a role in pathogenesis of hard tissue formation in odontogenic lesions.
Keywords: Calcification, odontogenesis, odontogenic tumour
How to cite this article: Thakur A, Siwach P, Agrawal RR. Hard tissue formation in odontogenic lesions associated with impacted tooth: Plausible pathogenesis. Indian J Dent Res 2020;31:782-3 |
How to cite this URL: Thakur A, Siwach P, Agrawal RR. Hard tissue formation in odontogenic lesions associated with impacted tooth: Plausible pathogenesis. Indian J Dent Res [serial online] 2020 [cited 2021 Jan 28];31:782-3. Available from: https://www.ijdr.in/text.asp?2020/31/5/782/306463 |
Odontogenesis is a complex process, which involves the molecular interaction between the epithelium and ectomesenchyme called as epithelium mesenchymal interaction (EMI). During tooth development there is the formation of dental lamina and enamel organ. Inner layer of enamel organ contains ameloblasts. During amelogenesis the ameloblast undergoes various stages, one of which is protective stage. During protective stage the fully formed tooth/enamel is covered by reduced enamel epithelium (REE). The function of the REE is that of protecting the mature enamel by separating it from the connective tissue until the tooth erupts. However, if prior to eruption enamel comes in contact with connective tissue, enamel may either get resorbed or covered by a layer of cementum. During the life cycle of ameloblasts, the epithelial enamel organ may retract from the cervical edge of the enamel. The adjacent mesenchymal cells may then deposit afibrillar cementum on the enamel surface.[1],[2],[3] After enamel formation, crown is covered by REE to prevent any interaction between enamel and ectomesenchyme. If any interaction occurs this leads to the formation of hard tissues.[1],[2],[3]
As considerable number of the odontogenic lesions (cysts and tumours) are associated with impacted tooth. REE acts as a source of origin, during the process of development of a lesion, disruption in REE may occur and lead to formed enamel coming in contact with ectomesenchyme leading to the formation of cementum like calcifications.[4],[5]
In addition, lesion arising apart from REE (epithelial rests in gubernaculum dentis or epithelial rests of Malassez), on progression may disrupt and fragment the REE. These different fragmented parts of REE may then itself act as a potential source of odontogenic epithelium as like other odontogenic remnants for various odontogenic lesions. These fragmented epithelium then independently interact with ectomesenchyme, leading to EMI. This further leads to an attempt to form multiple calcified structures (odontome/multiple calcification/enameloid/dentinoid).
We hereby tried to explore one of the possible pathogenesis behind the formation of hard tissue in odontogenic lesions associated with impacted teeth.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Kumar GS. Orban's Oral Histology and embryology. 13 th ed. India: Elsevier; 2011. p. 72-6. |
2. | Nanci A. Ten Cate's Oral Histology Development, Structure, and Function. 8 th ed. India: Elsevier; 2013. p. 205-16. |
3. | Hand AR, Frank ME. Fundamentals of Oral Histology and Physiology. 1 st ed.. Ames, Iowa: John Wiley&Sons; 2014. p. 69-79. |
4. | Reichart PA, Philipsen HP. Odontogenic Tumours and Allied Lesions. London: Quintessence Publishing Co Ltd.; 2004. p. 105-16. |
5. | Thakur A, Tupkari JV, Joy T, Hanchate AV. Adenomatoid odontogenic tumour: What is the true nature? Med Hypotheses 2016;97:90-3. |

Correspondence Address: Dr. Arush Thakur Department of Oral Pathology and Microbiology, Government Dental College and Hospital, St. George Campus, Near CST Station, Mumbai - 400001, Maharashtra India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijdr.IJDR_874_18

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