Age related and functional changes in dentin (Notes)
There are certain age related or functional changes that could happen in the dentin due to various external factors like attrition, abrasion, erosion, dental caries or operative procedures.
The changes that we would be discussing in this note would be the formation of
Tertiary dentin
Sclerotic dentin and
Dead tracts
Note
Please note that the formation of secondary dentin is also an age related change as it primarily starts to form after root completion and primary dentin formation. However, the deposition of secondary dentin is a physiologic process not dependent on external stimuli, unlike the changes listed above.TERTIARY DENTIN
External insults to the tooth like attrition, abrasion, dental caries, trauma or operative procedures could induce the formation of “tertiary dentin”
💡KNOW THY FACTS
Tertiary dentin is also known by various names such as reactionary dentin, reparative dentin, osteodentin and irregular secondary dentin.Types of Tertiary dentin
Tertiary dentin could be of two types depending on the whether odontoblasts survive or die as a result of the external stimuli.
During insults, odontoblasts may sustain damage, some may even die. Those that, despite damage, may recover and produce dentin. This dentin is termed as “reactionary dentin”.
However, in the event of the death of odontoblasts, undifferentiated mesenchymal cells from the pulp may be stimulated to become odontoblast like cells and may produce dentin. This dentin is termed “reparative dentin”.
Sometimes, the process of deposition of tertiary dentin may be so rapid, that the dentin producing cells may get entrapped within the matrix of dentin. This is called “osteodentin”.
WHY IS TERTIARY DENTIN WITH ENTRAPPED CELLS CALLED OSTEODENTIN?
During bone formation, the osteoblasts producing the organic matrix of the bone get entrapped within the matrix and become osteocytes (read the lesson on "Bone Histology" in the chapter "Bone"). Similarly dentin with entrapped cells resembles the bone organic matrix with entrapped osteocytes. This type of tertiary dentin is hence named osteodentin.Formation of odontoblast like cells
There are two schools of thought with regards to the formation of odontoblast like cells from the mesenchymal cells in the pulp.
Some odontoblasts that are formed during tooth development may remain dormant in the pulp. On stimulation, they may complete their life cycle and produce tertiary dentin.
The more accepted theory however is that, undifferentiated mesenchymal stem cells in the pulp differentiate to become odontoblast like cells. The stimulus for these stem cells is got from cytokines and growth factors that are locally synthesized in response to external factors.
Histology of tertiary dentin
It may have a regular tubular structure and be continuous with the secondary dentin.
However, tertiary dentin more often has very few tubules that are irregular or may sometimes have no dentinal tubules.
SCLEROTIC DENTIN
External factors like slowly progressing caries or attrition could damage odontoblastic processes and induce calcification of dentinal tubules.
Calcification of tubules could also occur in the presence of the odontoblastic processes.
The mineralization of several adjacent dentinal tubules could give them a glassy appearance and this region of dentin looks light and transparent when viewed in transmitted light. This is called sclerotic dentin.
The calcification of dentinal tubules and formation of sclerotic dentin is viewed as a protective response, as this portion of dentin is less permeable, effectively blocking out external irritants like bacteria and bacterial toxins. Hence sclerotic dentin may help prolong vitality.
Sclerotic dentin is usually seen in the elderly.
Sclerotic dentin occurs more often in the root dentin.
DEAD TRACTS
When odontoblast processes retract or odontoblasts are killed due to an external stimulus, the dentinal tubules would be empty.
Also, reparative dentin formed during these times may seal the tubules at the pulpal ends.
These empty tubules, during preparations of ground sections of teeth, may entrap air, reflect light and thus appear dark when viewed in transmitted light.
This portion of the dentin comprising of empty tubules with entrapped air, appearing dark in transmitted light are referred to as dead tracts.
HIGHLIGHTS - VIVA & ENTRANCE EXAM PERSPECTIVE
Tertiary dentin is also known by various names such as reactionary dentin, reparative dentin, osteodentin and irregular secondary dentin.
During insults, odontoblasts may sustain damage, some may even die. Those that, despite damage, may recover and produce dentin. This dentin is termed as “reactionary dentin”.
However, in the event of the death of odontoblasts, undifferentiated mesenchymal cells from the pulp may be stimulated to become odontoblast like cells and may produce dentin. This dentin is termed “reparative dentin”.
During reparative dentin formation, undifferentiated mesenchymal stem cells in the pulp differentiate to become odontoblast like cells. The stimulus for these stem cells is got from cytokines and growth factors that are locally synthesized in response to external factors.
Tertiary dentin more often has very few tubules that are irregular or may sometimes have no dentinal tubules.
The mineralization of several adjacent dentinal tubules could give them a glassy appearance and this region of dentin looks light and transparent when viewed in transmitted light. This is called sclerotic dentin.
Sclerotic dentin is less permeable and may help prolong vitality.
Sclerotic dentin occurs more often in the root dentin.
The portion of dentin comprising of empty tubules with entrapped air, appearing dark in transmitted light are referred to as dead tracts.
REFERENCES AND FURTHER READING
Berkovitz BKB, Hollan GR, Moxham BJ. Oral Anatomy, Histology and Embryology. 4th ed. Mosby Elsevier; 2009.
Nanci A. Tencate’s Oral Histology. Development, Structure and Function. 8th ed. Elsevier; 2013.
Kumar GS. Orban’s Oral Histology and Embryology.13th ed. Elsevier; 2011.
Avery JK. Oral development and Histology. 3rd ed. Thieme Medical Publishers; 2002.