Fully differentiated odontoblasts are 50–60 μm long columnar cells. Cell body and organelle distributions show polarization including one odontoblastic process containing a well-developed cytoskeleton and both exocytotic and endocytotic vesicles (Sasaki and Garant 1996). Terminally differentiated odontoblasts secrete the first layer of dentin (mantle dentin) and begin to move toward the center of dental papilla. During this movement, odontoblasts leave their process behind while forming into the dentin matrix. The dentin matrix mineralizes around the process and dentinal tubules forms. Dentin is constituted of thousands of dentinal tubules that cross over the dentin from the dentinoenamel junction to the pulp. Although odontoblasts display an epithelial appearance by their alignment at the periphery of pulp, the tight junctions between them play roles in cell polarization and differentiation processes rather than to permeability functions (Arana-Chavez and Massa 2004; Joao and Arana-Chavez 2004).

Other than mantle dentin, the differentiated odontoblasts continue to deposit different forms of dentins: circumpulpal, intertubular, and peritubular dentins. They are all formed up until the completion of root development and they are defined as primary dentin. However, odontoblasts deposit secondary dentin throughout life. While the secondary dentin secretion rate is slower than that of primary dentin, their structures are similar.

As stated before, odontoblasts are highly specialized, post-mitotic NC-derived cells. They produce the collagens and proteoglycans of the organic matrix of predentin and dentin. Odontoblasts also synthesize a variety of noncollagenous proteins, such as bone sialoprotein (BSP), dentin sialoprotein (DSP), dentin phosphoprotein (DPP), dentin sialophosphoprotein (DSPP), dentin matrix protein-1 (DMP-1), phosphoryn, osteocalcin, osteonectin, and osteopontin (OPN). DSPP, DSP, DPP, and DMP-1 are considered as being dentin-specific markers; however, they can be found in several other tissues with different roles. Hence, it has been shown that DSPP is not a tooth-specific protein and that dramatically different regulatory mechanisms governing DSPP expression are involved in tooth and bone (Qin et al. 2003; Suzuki et al. 2012). While DMP1 mutations have recently been shown to cause autosomal recessive hypophosphatemic rickets, tooth abnormalities have so far not been described in humans (Koshida et al. 2010). DSPP affects the mineralization of dentin more profoundly than DMP-1, whereas DMP-1 significantly affects bone mineralization and importantly controls serum phosphate levels (Suzuki et al. 2012). Although small integrin-binding ligands, the N-linked glycoproteins (SIBLINGs) group of extracellular matrix proteins involved in bone and teeth mineralization (family members include MEPE, DMP1, OPN, BSP, enamelin, DSPP, and statherin) are not currently regarded as being specific for dentin alone (Hao et al. 2005; Simon et al. 2009). Moreover there is limited information regarding the distinguishable biochemical features of bone and dentin.

Although there is detailed information about odontoblast differentiation during odontogenesis, little or no attention has been placed on the differentiation of the other cells of dental pulp. Fibroblasts are the predominant cell type in dental pulp. They are mostly found in the cell-rich zone of the pulp, which is localized beneath the subodontoblastic layer. Their particular role is maintaining the pulp matrix. They synthesize mainly type I and type III collagens, and a wide range of noncollagenous extracellular matrix components, such as proteoglycans and fibronectin. In the adult pulp, fibroblasts appear as flattened spindle-shaped cells. Fibroblasts are also included in the degradation of matrix components and thus are essential in the remodeling of pulp tissue (Okiji 2002).

Undifferentiated ectomesenchymal cells have been traditionally emphasized in dental literature. According to Nanci:

Since there is no known marker(s) for such an undifferentiated mesenchymal cell population, it is still unclear if dental pulp stem cells are part of primitive cell populations, which may be shown by undifferentiated mesenchymal cells.

Immunocompetent cells are normal residents in the connective tissue of the pulp and they respond to the situations that threaten tooth integrity, such as caries, tooth fracture, and cavity preparation. The human tooth is the target of a substantial number of oral bacterial agents that initiate the development of carious lesions (Okiji 2002). In the development of caries following enamel demineralization, dentin becomes exposed to the oral environment. This enables cariogenic bacteria to cause inflammation and subsequent immune system responses in the underlying dental pulp through the diffusion of by-products into dentin tubules (Farges et al. 2009). Dental pulp can also respond immunogenically to cavity preparation and restoration, but these immune responses are different to those caused by caries conditions (Yoshiba et al. 2003). Pulp retains its defense capacity even in aged pulps (Kawagishi et al. 2006).

Inflammatory and immune system cells, such as dendritic cells, neutrophils, histiocytes/macrophages, and T/B lymphocytes, are included in pulp. While B lymphocytes differentiate into antibody-secreting plasma cells (humoral immunity), T lymphocytes play the main part in specific immune responses. Cytotoxic T lymphocytes (CD8⁺) cause lysis of infected cells and helper T lymphocytes (CD4⁺) produce cytokines to orchestrate immunity. CD8⁺ cells bind Class I major histocompatibility complex (MHC) molecules in humans very polymorphically. These are designated as human leukocyte antigens, HLA, -A, and -C. HLA class I molecules are expressed in almost all cells of the body. Class II MHC molecules, on the other hand, bind to CD4⁺ molecules on T lymphocytes and they are HLA-DR, -DP, and -DQ in humans. In contrast to HLA type I, type II molecules are expressed in limited types of cells, mainly on dendrites and B lymphocytes. In intact teeth, they are distributed mainly in and around the layer of odontoblasts with dendritic profiles and are called pulpal dendritic cells (Shackelford et al. 1982; Okiji 2002).