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Pre-odontoblasts, Odontoblasts, or "Odontocytes"Institute of Dentistry, University of Oulu, Finland; markku.larmas{at}oulu.fi To the Editor: A recent report (Lu et al., 2007) inspired me to re-open a discussion on the biology and terminology of odontogenic cells, the importance of which was also highlighted by Kim and Simmer (2007). The life-cycle of the odontoblast—from pre-odontoblasts to secretory odontoblasts to transitional odontoblasts to aged (resting) odontoblasts—reflects the functional activity of the cell. Primary dentinogenesis proceeds during tooth eruption, which perhaps corresponds to the growth of long bones. Matrix formation is reduced during secondary dentinogenesis, and no resorption normally occurs in dentin. Subsequently, odontoblast activity can be up-regulated again during caries, as a reactionary tertiary dentinogenic response (Smith and Lesot, 2001). These changes in activity are reflected in alkaline phosphatase, which is 10- to 100-fold higher in the peri-odontoblastic layer prior to closure of the root apex, and which increases again under a caries lesion (Läikkö and Larmas, 1978). Alkaline phosphatase decreases in activity as osteoblasts differentiate into osteocytes (Blumer et al., 2006), the latter of which are viable for decades, in contrast to weeks for osteoblasts (Bonewald, 2002). There is also a striking similarity in the 3D-canicular systems in odontoblasts and osteocytes (Lu et al., 2007). These parallels lead me to propose that resting odontoblasts involved in secondary dentinogenesis should be re-named ’odontocytes’, at least in teeth with closed apices, on the basis of their function and properties, which correspond to those of osteocytes in bone. This proposal would mean that, after injury, ’odontocytes’ might participate in reactionary dentinogenesis (Smith et al., 1994) or, with more intense injury, undergo apoptosis when stem/progenitor cells (Gronthos et al., 2002) may differentiate into a new generation of odontoblast-like cells for reparative dentinogenesis. The temporal expression pattern of DMP-1 in odontoblasts (Lu et al., 2007) might correlate with a change in secretory activity of odontoblasts as they differentiate into ’odontocytes’. It would be interesting to know whether a similar expression pattern was observed in the apical area of the incisors in this study. With hereditary dentin defects (Kim and Simmer, 2007), the structural changes may reflect odontoblast/’odontocyte’ activity, which will also determine the size of the pulp chamber. Dentinogenesis Imperfecta I-III may arise from pathologic differences in the functional life-cycles of odontoblasts and osteoblasts: If pre-odontoblasts do not differentiate into odontoblasts, shell or thistle-tube teeth may result, and if odontoblasts do not differentiate into ’odontocytes’, premature pulpal obliteration may occur. Absence of odontoblast differentiation to ’odontocytes’ may also be physiologic in the case of continuously grown teeth with open apices, such as rodent and elephant incisors. REFERENCES
The authors reply
1 Texas A&M Health Science Center, Baylor College of Dentistry, Dallas, TX 75246, USA; Correspondence: * corresponding author, jfeng{at}bcd.tamhsc.edu In support of the concept of odontoblast differentiation into ’odontocytes’, we have compared early and late odontoblasts with osteoblasts and osteocytes, using two osteocyte markers, DMP1 and E11. Odontoblasts begin as polygonal cells that leave behind a single process in the dentin matrix with numerous branches, especially toward the dentin-enamel junction, highly reminiscent of the morphology of dendritic osteocytes within bone matrix.
Previously, we have shown that DMP1, an acidic extracellular matrix protein, is highly expressed in molar odontoblasts (Feng et al., 2002, 2003). To visualize the pattern of DMP1 expression in the incisor, we used a 10-day-old Dmp1 lacZ knock-in null mouse pup (in which the Dmp1 was replaced by a lacZ reporter) and a wild-type control. The freshly isolated incisors were stained with x-gal overnight, followed by fixation, acid decalcification, wax embedding, sectioning, and hematoxylin staining. Strong x-gal staining, reflecting high endogenous DMP1 expression, was detected in both odontoblasts and dentinal tubules in the Dmp1 lacZ knock-in null pup (Fig. 1a
Next, we examined and compared the expression pattern of E-11, a marker for newly formed osteocytes (Feng et al., 2006; Zhang et al., 2006), in both tooth and bone. Similar to Dmp1, E-11 is highly expressed in odontoblast processes and in the dendritic processes of osteocytes, with a very similar, if not identical, localization in both cell types (Fig. 2  ).
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, in the processes of odontoblasts and dendrites of osteocytes (Figs. 1  , 2), 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.
REFERENCES
Journal of Dental Research, Vol. 87, No. 3,
198-199 (2008)
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