to differentiate into mesenchyme stem–like cells capable of secreting both bone, collagen, and cementum and thus may be the progenitor cells of cementoblasts.4 It has also been argued that cementoblasts are not derived from either Hertwig's root sheath or ECRs but from mesenchymal cells of the dental follicle under the influence of ECRs.5 The epithelial cell rests may play an important role in periodontal regeneration.
Fig. 3.11 A undecalcified section through the root of a molar tooth (magnification × 500). The image has been selected from an area halfway toward the root apex showing the transition between acellular (ac) and cellular (c) cementum. The periodontal ligament (pl) has been removed during processing D, dentin.
3.6.3 Changes in Cementum with Aging
We have noted that continued eruption of the tooth, to accommodate for occlusal wear, may occur due to the deposition of new cementum to the root apex. This thickening of apical cementum appears to occur even if there is little tooth wear. It is a feature of aging and is one of the more reliable features used by forensic pathologists in estimating the age of a tooth or the body in which it is found.
3.6.4 Cementum Formation in Healing
The specific morphology of tooth support requires that fibers, embedded in the bone of the tooth socket, are also embedded in cementum covering the tooth root. Periodontal ligament fibers cannot adhere to the tooth root if the surface is covered by epithelium. Downgrowth of the junctional epithelium onto the surface of the cementum thus prevents fiber attachment to the root surface. If the tooth root is cleaned and the epithelium removed, it grows back during healing, faster than new cementum can form. Surgical techniques have been developed which prevent this downgrowth of epithelium. An artificial membrane is placed over the bone and root surface with the intention of preventing downgrowth of epithelium while healing occurs. This technique, called guided tissue regeneration, may promote the deposition of new cementum onto the root surface. The principle of guided tissue regeneration has been successfully applied in encouraging new bone formation around a dental implant, although the evidence for its success in regenerating periodontal ligament reattachment is less secure.
The new cementum is dependent on the differentiation of cementoblasts from cells dormant in the periodontal ligament. Only after new cementum is laid down against the root surface are fibers able to become incorporated in the new cementum and reattach the root to the alveolar bone. New bone then forms in the tooth socket, which traps the periodontal fibers, and a structural ligament is once more created.
The stimulus for the differentiation of new cementoblasts is provided by enamel matrix protein produced by epithelial cell rests. A derivative of these proteins from pigs has been shown to induce the differentiation of cementoblasts, fibroblasts, and osteoblasts. Clinical trials have shown that enamel matrix proteins are able to increase the success rate of reattachment of the tooth to the bony socket.6
Tooth displacement by an orthodontic appliance is followed by resorption of bone lining the tooth socket. This resorption is effected by osteoclasts. These are large multinucleate bone cells which appear to remove a lacuna (Latin lake) of bone around them. Once the tooth has repositioned, healing occurs first by migration of fibroblast-like cells into the resorption lacunae. After 3 weeks, new bone appears in the resorption defects. Associated with new bone formation after physiological tooth drift in rats are the noncollagenous bone proteins, osteonectin, osteopontin, and osteocalcin. It is likely that all three proteins are influential in controlling the balances of resorption and deposition of mineral in bone remodeling and healing (see Chapter 7.7.4 Tooth Repositioning).
Key Notes
Following periodontal disease, the reattachment of collagen fibers to the root surface is an essential step in repair of the entire periodontium. It is impossible without the regeneration of cellular cementum in which new fibers may be embedded. This regeneration cannot take place while the root surface is covered by a downgrowth of the epithelial attachment.
3.7 Junctional Epithelium
The junctional epithelium is an extension of the epithelium of the gingival sulcus but has some important differences. Firstly, unlike the epithelium of the gingival sulcus, it is physically attached to the surface of the tooth (▶ Fig. 3.12). Further, it is nonkeratinized, lacks the prominent rete ridges of gingival epithelium, and has no granular or keratin layer. The basal cells of the junctional epithelium are cuboidal and attached to the external basal lamina. The layer of epithelial cells above the basal lamina varies in thickness but is not more than about 20 cells thick. The unusual feature of junctional epithelium is that the surface cells are also attached to an internal basal lamina which in turn is attached to the enamel (or cementum) of the tooth. This attachment is achieved by hemidesmosomes at intervals along the basement membrane. This internal basement lamina is a product of the underlying cells and requires synthesis just as the synthesis of keratin would in the epithelium of attached gingiva.
The junctional epithelium forms a cuff of attachment around the tooth and is therefore of key importance as a barrier to the entrance of bacteria down the tooth surface and into the periodontium. We have seen the value of rapid turnover in epithelia, which allows regular shedding of the surface cells, along with any organisms that have obtained a foothold. The junctional epithelium exploits this process and turns over in just 4 to 6 days (in marmosets). The cells are not shed against the tooth surface but migrate through the layers above and emerge at the junction of the tooth and gingival sulcus. The junctional epithelium exploits other features of its structure to control the microorganism of dental plaque. The individual cells are not held close together (fewer desmosomes), and this allows neutrophil leukocytes to patrol in between the cells. Lymphocytes and monocytes may also occasionally be seen in the junctional epithelium. They are seen in much greater numbers if the gingiva becomes inflamed. Lastly, to help sweep away and disable microorganisms invading the junctional epithelium, a fluid exudate flows between the cells of the junctional epithelium and emerges into the gingival crevice (see Chapter 4.2.4 Gingival Crevicular Fluid).
Fig. 3.12 A diagrammatic representation of the junctional epithelium. The basal cells are attached to the external basement lamina (EBL) by hemidesmosomes. The inner basement lamina (IBL) forms the epithelial attachment to enamel, also via hemidesmosomes. The central cells of the epithelium are loosely attached and allow gingival fluid to flow outward into the gingival sulcus. C, cementum; D, dentin; E, enamel; l-break/>LP, lamina propria.
If the junctional epithelium is surgically removed, a new junctional epithelium forms and attaches to the tooth. It is presumably derived from the epithelium of the sulcus.
3.7.1 Loss of Epithelial Attachment
If plaque accumulates on subgingival surfaces of the tooth, there is a shift in the balance of microorganisms toward more gram-negative
