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Teeth and bones begin their development in humans within the 3rd to 8th weeks in utero when both dentinogenesis and ossification begin. Both are completed by late adolescence when bone modeling turns into bone remodeling and primary dentinogenesis into secondary dentinogenesis when the tooth is fully-formed (Fig. 1). A cartilage model directs endochondral ossification whereas teeth always develop in their final size, the onset being the crown cusp tips from which the growth continues in the direction of root, establishing the final dimensions of the tooth concerned.

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Figure 1. Schematic picture of developing (elongating and modeling) bone and forming (=developing and erupting) tooth (above) and remodeling adult bone and adult tooth (below) with the cells involved. Both mineralizing tissues are dissimilar in terms of embryology, molecular biology, and histology but may have some common features. Ameloblasts disappear after tooth emergence as do chondrocytes by apoptosis in the secondary growth plates of both epiphyses. Normally the dentition does not participate in mineral homeostasis and therefore osteoclasts are found in dentin only during pathological conditions, whereas microbes inside the tooth are always pathologic causing carious lesions in teeth.

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Though the timing of both is about the same, and both have many similar features, the cells are of different origin: bones are mainly mesodermal whereas craniofacial bony elements are derived from the neural crest and the paraxial mesoderm, which forms bone through both endochondral and intramembranous ossification. Alveolar bone provides the support for a functional dentition (Jain, 2010). Teeth are of either pure ectodermal (enamel forming ameloblasts) or of cranial neural crest (odontoblasts, cementoblasts/cementocytes) origin.

SCIENTIFIC NOMENCLATURE

  1. Top of page
  2. SCIENTIFIC NOMENCLATURE
  3. PRIMARY, SECONDARY, AND TERTIARY DENTINOGENESIS
  4. BONE MODELING AND REMODELING
  5. EXCEPTIONS OF TOOTH AND BONE GROWTH AND BLAST/CYTE TERMINOLOGY
  6. ACKNOWLEDGEMENT
  7. LITERATURE CITED

The terms of macroscopic or microscopic anatomy have not changed much in the last century. The scientific need for simple, stable, and internationally accepted systems for naming objects of the natural world has generated many formal nomenclatural systems. Probably the best known form of the Terminologia series: Anatomica in1998, Histologica in 2008, and Embryologica in 2009. All are the joint creation of the Federative International Committee for Anatomical Terminology and the member societies of the International Federation of Associations of Anatomists, collected and published by the Federative International Program on Anatomical Terminologies (FIPAT, 2012).

Because a rigorous, common language is the bedrock of science, recent discussions focused on the great variation of the names of cells connected to tooth ontogeny. This is because the official textbook terminology does not explain why some mammalian teeth are continuously growing, like elephant tusks, whereas most others are not (Larmas, 2008).

PRIMARY, SECONDARY, AND TERTIARY DENTINOGENESIS

  1. Top of page
  2. SCIENTIFIC NOMENCLATURE
  3. PRIMARY, SECONDARY, AND TERTIARY DENTINOGENESIS
  4. BONE MODELING AND REMODELING
  5. EXCEPTIONS OF TOOTH AND BONE GROWTH AND BLAST/CYTE TERMINOLOGY
  6. ACKNOWLEDGEMENT
  7. LITERATURE CITED

The basic dental cells are “odontoblasts” that form the bulk of the teeth. These cells are particular in the sense that their short mitotic life ends latest at the termination of the growth and eruption of teeth at adolescence. All other similar, long-living mammalian cells change their names when their stage turns from mitotic to post-mitotic, like osteoblast/osteocyte, chondroblast/chondrocyte in the primary growth plate, cementoblast/cementocyte, myoblast/myocyte, neuroblast/neurocyte/neuron, and so on. When an erythroblast turns to erythrocyte it even loses its nucleus.

Do adult odontoblasts transdifferentiate into “odontocytes” in teeth with closed tooth root apices (Larmas, 2008) as we now again suggest, or are they then with the present “informal nomenclature” “secondary odontoblasts” and after injury “tertiary odontoblasts” or “reactionary odontoblasts” as is suggested (Simon et al., 2011), or are they then “resting” or “old” odontoblasts” as textbooks and encyclopedia term them?

The most common feature of pulp repair in injury is the formation of tertiary dentin, a subgroup of which is reactionary dentin. It generally follows a mild injury, which “old” odontoblasts survive after the stimuli. The up-regulation of old odontoblast activity is clearly central to tooth response against injury.

More intense injury that leads to odontoblast/cyte death is followed by the formation of reparative dentin. Then more complex defense and healing responses occur, with recruitment of stem/progenitor cells first reported by Gronthos et al. (2000), their differentiation to odontoblast-like cells, and subsequent up-regulation of secretory activity which is called reparative dentinogenesis.

We are not sure whether odontoblasts can normally be activated. We have the feeling that primary dentinogenesis always occurs at its maximum speed because the tooth eruption time-table is relatively constant all over the world. Response by (primary) odontoblasts during dentinogenesis may also mean a reduction of their secretory activity, and later, even cell death (Larmas, 2001).

The historical reason why an odontoblast has not changed its name is partly due to the lack of information on the activity of the marker enzyme, alkaline phosphatase during the time of nomenclature creation (Larmas, 2001), and partly anatomical: odontoblasts are not trapped in any lacuna like are osteoblasts when turning into osteocytes. At the closure of human root apex alkaline phosphatase activity is reduced in all peripulpal odontoblasts in the dentin–pulp complex (Läikkö and Larmas, 1978, 1980) indicating a similar change that happens in osteoblasts in transdifferentiating into osteocytes in bone lacunae.

When reanalyzing the old histochemical pictures (Larmas and Kantola, 1973) using the frame of present knowledge, it can summarized that: (1) alkaline phosphatase activity is high in the developing apex area of tooth root, both in the odontoblasts and cementoblasts (Fig. 2B,C), (2) alkaline phosphatase activity disappears from the odontoblasts under an advanced carious lesion (Fig. 2C); (3) alkaline phosphatase activity is induced in pulpal fibroblasts/progenitor/stem cells surrounding the inflamed pulp horn (Fig. 2C), where the (4) inflammation is indicated by an elevated aminopeptidase activity (Fig. 2D). Evidently alkaline phosphatase is involved in tooth development and response against carious attack.

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Figure 2. A: A microradiograph of a developing human molar tooth with an advanced carious lesion. Undecalcified frozen section of an extracted human molar tooth. B: Localization of alkaline phosphatase activity in the tooth. C: Localization of alkaline phosphatase activity under the advanced carious lesion with pulp perforation and pulpal inflammation. D: Aminopeptidase activity in the fibroblasts/progenitor/stem cells or inflammatory cells in the inflamed pulp horn. The picture is reconstructed from the original slides published by Larmas and Kantola (1973) in Acta Odontol Scand 31:179–185.

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However, differentiated odontoblasts could not be identified solely by one unique phenotypic marker, like are the alterations in alkaline phosphatase activity. The combination of expression of dentin phosphoprotein (DPP), dentin sialoprotein (DSP), dentin matrix protein 1 (DMP1), and nestin may be valuable for the assessment of these cells (Quispe-Salcedo et al., 2012). Wu et al. (2011) speculated that extracellular DMP1 may be a physiological regulator of osteoblast/odontoblast-specific genes. Indeed, the DMP1 null mice revealed that DMP1 is not only required for the formation of both the organic and inorganic components of dentin, but its absence also results in changes in osteocyte morphology, reduced bone elasticity, and progressive morphological bone abnormalities concomitant with aging.

Odontoblasts in dentin and osteocytes in bone contain dendritic processes. To test whether their dendrites share a common feature, Lu et al. (2007) compared their cellular morphology as visualized using scanning electron microscopy. Both cells shared an identical dendritic canalicular system and express extensive processes forming a complex network within the mineralized matrix. The remarkable similarities in morphology and the 3D canalicular systems in both odontoblasts and osteocytes (Lu et al., 2007) together with a very similar expression pattern of two osteocyte markers, DMP1 and E-11, a marker for newly formed osteocytes (Feng et al., 2006) in the processes of odontoblasts and dendrites of osteocytes (Ma et al., 2008) strongly support the parallel differentiation pattern of osteoblasts into osteocytes in bone and odontoblasts into “odontocytes” in teeth. This new concept of an “odontocyte” supports the hypothesis that osteocytes and “odontocytes” may share other properties and functions. Developing these new concepts should aid in the understanding of the physiological and pathological roles of these two cell types in bone and teeth.

This view is not shared by all researchers. Recently, the autophagic-lysosomal system of human odontoblasts was characterized with transmission electron microscopy and immunocytochemistry (Couve and Schmachtenberg, 2011). They demonstrated the presence of large autophagic vacuoles in coronal odontoblasts from young patients and a successive increase in their number with aging. They suggested that autophagic activity in odontoblasts is a fundamental mechanism to ensure turnover and degradation of subcellular components. In adult teeth, they termed this condition as an “old odontoblast” stage. Dr. Couve is the farther of this textbook term that is based on his historical observations with 12-year-old children (Couve, 1986).

BONE MODELING AND REMODELING

  1. Top of page
  2. SCIENTIFIC NOMENCLATURE
  3. PRIMARY, SECONDARY, AND TERTIARY DENTINOGENESIS
  4. BONE MODELING AND REMODELING
  5. EXCEPTIONS OF TOOTH AND BONE GROWTH AND BLAST/CYTE TERMINOLOGY
  6. ACKNOWLEDGEMENT
  7. LITERATURE CITED

Chondroblasts assume the shape of the future bone. The area surrounding the cartilage starts to give rise to osteoblasts. As a result a thin layer of bone is formed around the cartilage model and the chondroblasts turn into chondrocytes. Subsequently, the matrix surrounding undergoes calcification. The cartilaginous growth plate forms at the primary ossification center. The calcified matrix slows the diffusion of nutrients causing the death of the chondrocytes. This leaves large holes where blood vessels can penetrate.

Skeletal development and growth (bone modeling) and its maintenance in post-natal life in response to local and systemic stimuli (bone remodeling) require coordinated activity among osteoblasts, osteocytes, and osteoclasts, in order to meet the ongoing needs of structural integrity, mechanical competence, and maintenance of mineral homeostasis (Civitelli, 2008). One mechanism of cell–cell interaction is via direct cell–cell communication via gap junctions. These are transmembrane channels that allow continuity of cytoplasms between communicating cells (Civitelli, 2008).

Some osteoblasts become osteocytes by inversion of their own matrix secretion or by entrapment through neighboring osteoblasts (Marks and Popoff, 1988). Osteocytes are terminally differentiated old osteoblasts which make up 90% of the cells present within bone (Zhu et al., 2011). They are distinctive and isolated cells that are embedded within the bone matrix. Although the precise actions of osteocytes in bone have yet to be fully elucidated, these cells play pivotal mechanomodulatory roles in directing bone formation and bone resorption in response to load-bearing (Burger and Klein-Nulen, 1999). Bone cells in tissue culture express more alkaline phosphatase in response to mechanical loading by vibration (Tirkkonen et al., 2011).

EXCEPTIONS OF TOOTH AND BONE GROWTH AND BLAST/CYTE TERMINOLOGY

  1. Top of page
  2. SCIENTIFIC NOMENCLATURE
  3. PRIMARY, SECONDARY, AND TERTIARY DENTINOGENESIS
  4. BONE MODELING AND REMODELING
  5. EXCEPTIONS OF TOOTH AND BONE GROWTH AND BLAST/CYTE TERMINOLOGY
  6. ACKNOWLEDGEMENT
  7. LITERATURE CITED

The sizes of both primary and permanent teeth are predestinated: both start their development on the dimensions of the final size of the crown of tooth, after which only elongation occurs until puberty (Fig. 1). Evidently they are the only organs that attain their final width at birth. In bones the situation is different. In terms of embryology, molecular biology, and histology, the two mineralizing organs are barely comparable. Even functionally they are different. The cartilaginous skeleton is needed during the birth of an offspring but it is replaced by growing (in length and width) bones because no plastic cartilage is needed after the delivery, but it is important in directing the growth of bones.

In addition to the odontoblast the other exception from the blast/cyte terminology is connected to the growth of long bones: The cartilaginous growth plate forms at the secondary ossification centers of both epiphyses. The cells of the growth plates proliferate rapidly and are termed “round chondrocytes” and differentiate even more rapidly proliferating to “flat chondrocytes” then large to “hypertrophic chondrocytes” until they undergo apoptosis. The growth plate will then be replaced by bone. The suffix “cyte” is now used in mitotic cells. Although chondroblast is still commonly used to describe an immature chondrocyte, use of the term is according to Wikipedia discouraged, for it is technically inaccurate since the progenitor of chondrocytes (which are mesenchymal stem cells) can also differentiate into osteoblasts (but never directly to mesenchymal osteocytes). Our comment is that this sounds confusing: Would it not be more consistent to call round and flat chondrocytes, more correctly round chondroblasts and flat chondroblasts?

Therefore, should the harmonization of cells and terms of dentition and cartilage then be on the agenda of Federative International Committee for Anatomical Terminology or International Federation of Associations of Anatomists like was the problem of planets in the International Astronomical Union. Its General Assembly determined in 2006 that Pluto is not a planet but is a “dwarf planet”.

Renaming a mitotic chondrocyte to chondroblast and/or a resting/old/secondary odontoblast simply to odontocyte does not deny that they are two states of the same cells and therefore this decision may not lead the reader astray.

ACKNOWLEDGEMENT

  1. Top of page
  2. SCIENTIFIC NOMENCLATURE
  3. PRIMARY, SECONDARY, AND TERTIARY DENTINOGENESIS
  4. BONE MODELING AND REMODELING
  5. EXCEPTIONS OF TOOTH AND BONE GROWTH AND BLAST/CYTE TERMINOLOGY
  6. ACKNOWLEDGEMENT
  7. LITERATURE CITED

The authors received no financial support and declare no potential conflicts of interest with respect to the authorship and/or publication of this article.

LITERATURE CITED

  1. Top of page
  2. SCIENTIFIC NOMENCLATURE
  3. PRIMARY, SECONDARY, AND TERTIARY DENTINOGENESIS
  4. BONE MODELING AND REMODELING
  5. EXCEPTIONS OF TOOTH AND BONE GROWTH AND BLAST/CYTE TERMINOLOGY
  6. ACKNOWLEDGEMENT
  7. LITERATURE CITED
  • Burger EH, Klein-Nulen J. 1999. Responses of bone cells to biomechanical forces in vitro. Adv Dent Res 13:9398.
  • Civitelli R. 2008. Cell–cell communication in the osteoblast/osteocyte lineage. Arch Biochem Biophys 473:188192.
  • Couve E. 1986. Ultrastructural changes during the life cycle of human odontoblasts. Arch Oral Biol 31:643651.
  • Couve E, Schmachtenberg O. 2011. Autophagic activity and aging in human odontoblasts. J Dent Res 90:523528.
  • Feng JQ, Ward LM, Liu S, Lu Y, Xie Y, Yuan B, Yu X, Raucht F, Davis SI, Zhang S, Rios H, Drezner MK, Quarles LD, Bonewald LF, White KE. 2006. Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism. Nat Genet 38:13101315.
  • FIPAT, Federative International Program on Anatomical Terminologies. 2012. http://www.unifr.ch/ifaa/Public/EntryPage/ViewSource.html. Accessed on November 19, 2012.
  • Gronthos S, Mankani M, Brahim J, Robey PG, Shi S. 2000. Postnatal human dental pulp stem cells (DPSCs) in vitro and in vivo. Proc Natl Acad Sci USA 97:1362513630.
  • Jain V. 2010. Neural crest contribution to dental pulp stem cells/progenitor cells and craniofacial structures: alveolar processes, tongue and temporomandibular joint. http://etd.uthsc.edu/WORLD-ACCESS/Jain/2010-025-Jain.pdf. Accessed on December 15, 2012.
  • Läikkö I, Larmas M. 1978. Phosphomonoesterase activity in dentine of sound and carious human teeth. Caries Res 12:148158.
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  • Larmas M. 2001. Odontoblast function seen as the response of dentinal tissue to dental caries. Adv Dent Res 15:6871.
  • Larmas M. 2008 Pre odontoblasts, odontoblasts or “odontocytes”. J Dent Res 87:198.
  • Larmas M, Kantola S. 1973. A histochemical study of arylaminopeptidases and alkaline phosphatases in sound and carious human teeth. Acta Odontol Scand 31:179185.
  • Lu Y, Xie Y, Zhang S, Dusevich V, Bonewald LF, Feng JQ. 2007. Dmp1 targeted Cre expression in odontoblasts and osteocytes. J Dent Res 86:320325.
  • Ma D, Barragan-Adjemian C, Xie Y, Lu Y, Bonewald LF, Feng JQ. 2008.The authors reply. J Dent Res 87:199.
  • Marks SC, Jr., Popoff SN. 1988. Bone cell biology: the regulation of development, structure, and function in the skeleton. Am J Anat 183:144.
  • Quispe-Salcedo A, Ida-Yonemochi H, Nakatomi M, Oshima H. 2012. Expression patterns of nestin and dentin sialoprotein during dentinogenesis in mice. Biomed Res 33:119132.
  • Simon SRJ, Berdal A, Cooper PR, Lumley PJ, Tomson PL, Smith AJ. 2011. Dentin-pulp complex regeneration: from lab to clinic. Adv Dent Res 23:340345.
  • Tirkkonen L, Halonen H, Hyttinen J, Kuokkanen H, Sievänen H, Koivisto AM, Mannerström B, Sándor GK, Suuronen R, Miettinen S, Haimi S. 2011. The effect of vibration loading on adipose stem cell number, viability and differentiation toward bone-forming cells. J R Soc Interface 8:17361747.
  • Zhu D, Mackenzie NC, Millán JL, Farquharson C, MacRae VE. 2011. The appearance and modulation of osteocyte marker expression during calcification of vascular smooth muscle cells. PloS One 6:e19595.
  • Wu H, Ning-Teng P, Jayaraman T, Onishi S, Li J, Bannon L, Huong H, Close J, Sfeir C. 2011. Dentin matrix protein (DMP1) signals via cell surface Integrin. J Biol Chem 286:2946229469.