Odontoblasts are postmitotic cells, organized as a layer of palisaded cells along the interface of dentin and pulp of the tooth. The function of odontoblasts in a tooth includes the formation of physiological primary and secondary dentin, synthesis of Type I collagen, mineralization by secretion of proteoglycans and noncollagenous proteins. Furthermore, they synthesize reactionary dentin in response to the pathological conditions for the maintenance of dentin, acts as a sensor to bacterial invasion during caries process and subsequently initiate pulpal immune and inflammatory response. In addition to this, they aid in the mediation of tooth pain and sensation due to the presence of ion channels implicated in mechano-transduction or nociception. Being prone to injuries, odontoblasts; when injured by various etiological factors lead to the emergence of oral diseases.[1,2,3]
Development of Odontoblasts
Derived from cranial neural crest cells, odontoblasts first appear from 17 to 18 weeks in utero at sites of tooth development and are present till the tooth is completely necrosed due to direct invasion by bacteria or chemicals or indirectly through the factors such as heat or trauma during dental treatment procedures. During the initial phase of development, odontoblasts contain tomes fibers.
Functions of Odontoblasts
- The primary function of odontoblasts is to produce dentin throughout the life of the tooth
- They are also engaged in the repair of dentin
- They act as pain receptors and defensive cells in the dental pulp
- The odontoblasts also play an important secondary role in sensation of the tooth
- They aid in the secretion of intertubular and peritubular dentin (the dentin surrounding odontoblastic process) that forms the dentinal tubule
- They help in the general maintenance of both the dentinal tubule and dentinal fluid
- To secrete sclerotic dentin upon carious attack to block off dentinal tubules, slowing the progress of the attack (air space above blockage is known as a dead tract)
- To channel the signals of attack to the odontoblastic cell body, thus initiating secretion of reactionary dentin
- To act as the cellular component of the dental temperature sensing system either by sensing temperature changes directly or by detecting hydrokinetic forces of fluid movement in the tubules or a combination of both.[5,6]
Mechanosensory Role of Odontoblasts
Along with the external stimuli sensation, odontoblasts cause transient changes inside the pulp. Dentinal fluid inside the dentinal tubules' aids in the detection of this movement. Although it has been difficult to properly examine, previous research indicates elevated concentrations of potassium as compared to the control serum in the dentinal fluid.
There is a strong association of nerves with odontoblasts observed. These include trigeminal nerve fibers form the sensory axonal network around odontoblasts, the presence of primary cilium (an organelle involved in sensory transduction) has been regularly identified, which is said to sense pulp microenvironment; as Odontoblasts, thus, have a sensory function due to mechano-sensory receptors through axonal signal transduction pathways.
Recognition of Noxious Stimuli
Odontoblasts possess several ion channels such as voltage-gated sodium channels, that participate in nociception and signal propagation. Recently, the expression of several members of the transient receptor potential superfamily of ion channels has been detected in odontoblasts, which indicates the ability of odontoblasts to detect and/or transduce sensory physiological stimuli, such as thermal, mechanical, and chemical stimuli.
Odontoblasts, due to also the presence of acid-sensing ion channels, detect pH fluctuations. Furthermore, TREK-1, a mammalian mechanosensitive K + channel, which is involved in polymodal pain perception immune cells, provide resistance of epithelial and mucosal surfaces to microbial invasion. Its presence in odontoblasts suggests the contribution of these molecules in pulpal host defence mechanisms.
Odontoblasts are principal and specialized cells of the pulp-dentin complex. Their cell bodies lie at the periphery of the pulp chamber, with projection of their protoplasmic processes into the dentinal tubules. The appearance varies as they proceed from crown to the root apex. In the crown, they appear is tall columnar, become cuboidal in the middle region of the root and flat spindle-shaped near the apex of tooth. Odontoblastic cells are columnar and measure approximately 50 mm in height, in the crown of a fully developed tooth.
Microscopically, odontoblasts have an oval nucleus and a tomes fiber. Each odontoblast is separated from one another by intercellular condensation of the terminal bars. These terminal bars are connected with each other and with adjacent cells of the pulp by intercellular bridges. The cell processes of odontoblasts in dentin are long with few short lateral processes.
The number of odontoblasts corresponds to the number of dentinal tubules. The morphology of odontoblasts reflects their functional activity and ranges from an active synthetic phase to a quiescent phase.
In light microscopy, an active cell appears elongated and possesses a basal nucleus, a basophilic cytoplasm and a prominent Golgi zone. A resting cell by contrast, is stubby with little cytoplasm, and has hematoxyphilic nucleus.
Transmission electron microscopy
Odontoblasts contain ribosomes, Golgi apparatus, mitochondria, and cytoplasmic granules. Golgi saccules exhibit cylindrical and spherical distention where the collagen molecule is processed. It also contains potassium, calcium, phosphorus, glycogen, glycoprotein, alkaline phosphatase, and lipids.
The organelles of an active odontoblast are prominent, consisting of numerous vesicles, an endoplasmic reticulum, a well-developed Golgi complex located on the dentinal side of the nucleus and numerous mitochondria, scattered throughout the cell body. The nucleus contains an abundance of peripherally dispersed chromatin and several nucleoli. The pathway for collagen synthesis within the odontoblasts and its intracellular and extracellular assembly is similar to that of the fibroblasts. Spherical and cylindrical distentions are implicated while processing the procollagen molecule. The cylindrical distensions bud off as secretory granules, exhibiting a characteristic elongated shape and electron density, followed by its transportation toward the odontoblasts process, where their content is released.
Scanning electron microscopy
The odontoblast processes in the tubules are found within a distance from the pulp, equalling about one quarter the total length of the tubule. The process is more than 0.4 mm from the pulp and is not seen beyond 0.7 mm from the pulp. The process is tube like and almost completely fills the tubule in the predentin-dentin area and up to a distance of 0.2 mm from the pulp.
In the predentin-dentin area, the processes are surrounded by a thin membrane-like structure. Internally, the dentin tubule wall is coated with an amorphous substance containing a few circumferentially and longitudinally arranged fibers with an absence of nerve fibers. Odontoblasts are tall bowling pin-shaped cells border the pulp and form a tight layer against predentin. The process is surrounded by the collagen fibrils of predentin. The fibrils are associated intimately with the process, and in certain areas, imprint the membrane odontoblastic junctions between odontoblasts.
Theories of dentin sensitivity and aging process with the architecture of odontoblasts and its surrounding structures have been studied using confocal microscopy.[15,16]
Kagayama M studied the structures of dentinal tubules by undecalcified ground sections of human teeth, stained with alizarin red in 0.1% KOH aqueous solution, and examined by confocal microscopy.
Goracci et al., used both; scanning electron microscopy (SEM), confocal laser scanning microscopy (CLSM), and light microscopy, for the analysis of the relationship between hard dental tissues (dentin) and soft tissues (pulp). Membranous structures were observed by CLSM to extend from the pulp to the dentino-enamel junctions (DEJ), even in the zones where necrosis of the odontoblast occurred. The study confirmed the presence of the lamina limitans of peritubular dentin. SEM analysis confirmed the presence of tubular structures only in the inner third of the dentin (toward the pulp).
Third Dimension of Odontoblasts
In a three-dimensional (3D) animation view, odontoblasts reside inside the dentinal tubules representing millions of tunnels-like structures within the dentinal wall. These tunnels begin at pulpal ends and open onto DEJ and cemento-enamel junctions. Odontoblasts have a cell body and its process [Figure 1]. The cell body is present at the pulpal end and only the process enters the tubule [https://links.lww.com/JSCI/A1].
Odontoblasts in oral diseases
There are several ways by which odontoblasts get affected.
There is odontoblast degeneration characterized by decreased amounts of cytoplasm, disorganization of the cell layers, and lack of nuclear details.
Odontome is characterized by proliferation and disorganized arrangement of odontogenic tissues including odontoblasts. In compound odontoma, the tissues are organized resembling the shape of a tooth, and in complex odontoma, there is the presence of disorganisation of tissues. Since it is a benign tumor, proliferating cells are of normal morphology.
Here, odontoblastic processes are unprotected by an enamel layer and cementum is exposed to the environment. The surrounding dental lymph creates turbulence and causes lot of sensitivity.
Developmental disorders of dentin
Physical, chemical, and nutritional disturbances can negatively impact the function and vitality of the cell lineages residing in the developing tooth germs. When odontoblasts are severely injured and undergo apoptosis, dental pulp cells may differentiate into odontoblast-like cells and resume the production of dentin. Depending on the stage of formation, the intensity and duration of the insult, the resulting dentin defect may be localized or limited to the primary or the permanent dentition. The disturbances of dentinogenesis often result in structural malformation and in severe cases, alteration of tooth color. Although the etiology is unknown, histopathological evidence suggested that these lesions are not carious in nature but resorptive.[21,22,23]
Hereditary dentin defects
Hereditary dentin defects (HDDs) are classified as three types of dentinogenesis imperfecta [DGI-I (DGI-II and DGI-III and two types of dentin dysplasia DD-I and DD-II. Dentinogenesis imperfecta shows altered dentin, with the atypical granular matrix demonstrating an interglobular calcification.
The genetic causes of most HDDs correlate with the protein composition of dentin: type I collagen and dentin sialophosphoprotein-derived proteins. All these proteins are the product of odontoblasts. The proteins are defective in nature.[23,24]
Age-related changes of the dental pulp complex and their relationship to systemic aging
Odontoblasts are dentin-secreting cells that survive for the whole life of a healthy tooth. Once teeth are completely erupted, odontoblasts transform into a mature stage that allows for their functional conservation, while maintaining the capacity for secondary and reactionary dentin secretion. Odontoblasts are also said to transmit sensory stimuli from the dentin-pulp complex and aid in in the cellular defence against pathogens. Autophagic-lysosomal system that ensures organelle and protein renewal, thereby sustaining their longevity. However, progressive dysfunction of this system caused by lipofuscin accumulation reduces the fitness of odontoblasts and eventually impairs their dentin maintenance capacity. Understanding the biological basis of age-related changes in human odontoblasts is crucial to improving tooth preservation in the elderly.
The most significant hazard to the developing permanent successor occurs when it is directly involved in the trauma, causing crown or root dilaceration, or displacement of the tooth germ, results in impacted teeth and eruption disturbances leading to abnormal direction of dentin formation due to shifting of odontoblasts by an injury.
Odontoblasts in odontogenic tumors
Odontogenic tumor classifications generally divide the odontogenic tumors into groups, which variably recapitulate the features of their putative embryonic precursor tissues. Thus, there is an epithelium group, ectomesenchyme group and a mixed group exhibiting both epithelial and ectomesenchymal components.
However, odontomas represent developmental anomalies or hamartomas and not neoplasms. In the rare cases, where dentin is found within a genuinely expansile lesion (odontoameloblastoma, ameloblastic fibrodentinoma, or ameloblastic fibrodentinoma), the neoplastic element is thought to be the epithelial or ectomesenchymal component with dentin formation due to inductive changes in response to epithelium. Thus, mixed odontogenic tumors, benign or malignant, which include neoplastic odontoblasts are rare, if indeed, they even exist, odontoblast neoplasia or odontoblasts showing suggested preneoplastic changes have never been described.[27,28,29]
Rickets (Vitamin D resistant)
Histological examination of the teeth involved in familial hypophosphatemia often reveals poorly mineralized globular dentin, and tubular defects extending close to the DEJ. These cesses of the primary teeth. As expected of an X-linked condition, a spectrum of manifestations ranging from minimal to severe has been described.
A true “dentinoma,” one of the rare types of odontomas has been reported. The tumor develops at the apex defects predisposing exposure and infection of the pulp following enamel removal due to caries or attrition. The origin of such a growth could be due to the possibility of its development, as a result proliferation of connective tissue and of the Hertwig's epithelial root sheath is taken into consideration. The epithelial remnants induce the undifferentiated cells of the connective tissue to transform into odontoblasts and to produce dentin.
The microscopic examinations of the tumor consist mainly of dentin. In the periphery, the degree of calcification does not seem to be as good as in the central areas. In fact, in numerous regions, interglobular dentin can be appreciated. In some areas of the connective tissue of the nutrient canals, odontoblast-like cells can be observed.[30,31]
Dens in dente
When the odontogenic cells invaginate from the occlusal portion into the pulp, it start forming dental tissues inside the pulp chamber including odontoblasts.
When enamel is lost and dentin is exposed, it leads to sensitivity and caries. Open tubules are injurious to odontoblastic processes and lead to its degeneration.
When during the development of tooth, the developing dentinal layer is lost at places and overlying cementum doesn't form on it. Clinically, it is seen as perforation on the external surface of the root.[33,34]
Mature teeth are always subjected to injuries. When the odontoblastic layer gets traumatized the overlying dentin and enamel undergoes resorption due to internal systemic factors, it is seen as perforations.
Dentinogenic ghost cell tumor
This benign odontogenic tumor exhibits a lot of dentioid like depositions.
Endodontic Perspectives of Odontoblasts
Odontoblasts have a sensory and mechano-transduction role to detect external stimuli that challenge the dental pulp.[13,36] On detection, odontoblasts stimulate the innate immunity by activating defence mechanisms, which represents a key in the healing and repair mechanisms of the tooth. A better understanding of the role of odontoblasts within the dental pulp complex will encourage the biological management to remove the cause of the insult to the dental pulp, modulate the inflammatory process, and promote the healing and repair capabilities of the tooth.
Currently, the use of conventional dental pulp medicaments, bioactive molecules, epigenetic modifications, and tissue engineering are used. Hence, regenerative medicine methods prove an effective in incipient and experimental stages of the lesion. Recently, a population of mesenchymal stem cells has been isolated from dental pulp tissue, and these cells are generally referred to as dental pulp stem cells (DPSC).[4,37]
Since, dental pulp exhibits multipotency, they can differentiate into osteoblasts, adipocytes, and neuronal cells. They were first isolated from the pulp tissue of permanent human teeth and were designated postnatal DPSC.
The location of these cells is unknown as they lack specific markers. Conservation of dentin pulp complex is important as they provide longevity to the tooth. The pulp revascularization procedure, where there is regeneration of pulp tissue by host blood, bone marrow, or periodontal ligament-derived stem cells in immature nonvital teeth, is one of the current hot topics in clinical endodontics.
In this procedure, hard-tissue formation is observed in successful cases, but the resultant hard tissue is not always dentin-like and can exhibit a bone/cementum-like structure instead. Thus, regeneration of the dentin/pulp complex via the transplantation of DPSC into the root canals of nonvital teeth has recently gained much attention as a future therapeutic approach.
The applications such as root canal revascularisation, pulp implants, injection inside the root canal of cell-seeded hydrocolloid bio-gels, cells stimulation with growth factors for in-situ cell activation, and gene therapy are being researched in the hope of developing new endodontic treatments due to the benefit of presence of pluripotent cells in tooth.[5,41]
Summary and Conclusion
Odontoblasts in addition to the formation of dentin are found to support the notion that odontoblasts also function as nociceptors and defensive cells in the dental pulp. The regeneration of odontoblasts from DPSC takes place due to damage of odontoblasts, responding to the severe noxious stimuli. The damage of DPSC occurs due to molecular and physical injuries leading to the occurrence of various diseases. Nevertheless, the regenerating capacity of pulp proves to be a promising future for replacement of the damaged odontoblasts. The addition of third dimension to its histology will create a new dimension in teaching methods.
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Conflicts of interest
There are no conflicts of interest.
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