Proceedings of the Finnish Dental Society. Suomen Hammaslaakariseuran toimituksia最新文献

The distribution and subcellular localization of nerve growth factor receptor (NGFR) in human teeth has been investigated by immunohistochemistry at the light and electron microscopic levels. Many nerves in the dental pulp were intensely immunoreactive for NGFR. The pattern of distribution was largely similar to that of nerve fibers demonstrated by immunostaining for neurofilament protein (NFP), the most universal marker protein for pulpal nerves. In the predentin and dentin, more nerve fibers were intensely immunoreactive for NGFR than were demonstrable with NFP-antibodies. Immunoelectron microscopy showed that the NGFR-immunoreactivity was localized on the axoplasmic membrane in unmyelinated axons and on the outside of accompanying Schwann cells. No NGFR-immunoreactivity was found on the axons of myelinated nerves nor their supporting cells.

The present investigation describes how intradental afferent C-fibers can be identified and characterized in the anaesthetized cat. Functional single fibers innervating the lower canine tooth were recorded from filaments split from the inferior alveolar nerve. Fibers responding to monopolar electrical stimulation of the tooth were classified as slowly and fast conducting according to their conduction velocity (c.v.). The axonal c.v. was determined for 31 slowly conducting fibers by electrical stimulation of the nerve. Sixty-eight percent of these proved to be C-fibers. The slowly conducting fibers had higher activation thresholds, smaller amplitudes and longer durations of the action potentials than the fast conducting fibers. Many of the fast but none of the slowly conducting fibers were repetitively activated by a single stimulus pulse. The highest frequency at which the fibers responded to every stimulus pulse was much lower for the slowly than for the fast conducting fibers. Most of the slowly conducting intradental fibers tested were activated by both hot and cold stimulation of the tooth, by pressure applied to the pulp chamber and by the application of KCl or bradykinin to the pulp. Eight C-fibers responded to mechanical stimulation of the pulp. For some fibers the response magnitude correlated with the stimulus intensity. Many slowly conducting intradental fibers developed an ongoing discharge after heat and pressure stimulation. The results indicate that there exists in the dental pulp of the cat afferent C-fibers that resemble polymodal C-nociceptors. They might be involved in the generation of the dull aching pain present in inflammatory conditions of the pulp. The activation of intradental C-fibers in pulpitis might result either from the elevated pressure and/or by sensitization of the C-fiber endings by inflammatory substances released.

Extracted human teeth were collected from young (20-28 yrs) versus old (45-69 yrs) patients. The teeth were divided into carious and noncarious groups. Slabs were created from the mid-coronal occlusal dentin. Carious lesions were excavated and the smear layers on both normal and excavated carious dentin were removed with 37% phosphoric acid (1 min). The permeability (hydraulic conductance) of old normal dentin was only 20% of that obtained in young normal dentin but all of the specimens were permeable. Young carious dentin was only 14% as permeable as young normal dentin and only 1 out of 7 specimens was not permeable. All 7 specimens of old carious dentin were impermeable. Scanning electron microscopy of old and carious dentin exhibited far more intratubular crystals than normal dentin, providing a structural basis for the functional observation.

The reactions of sensory nerves to restorative procedures can be classified as immediate, early and late. For each of these, the neural response depends upon the severity of pulpal injury and the stages of inflammation and healing. Immediate responses in the first few minutes include destruction of nerve fibers in the injured dentin and pulp, hypersensitivity of surviving fibers, release of neuropeptides into the pulp and neurogenic inflammation. Early responses occur during the first few days after cavity preparation, with nerve fibers sprouting in the surviving pulp and gaining increased axonal transport and neuropeptide contents. Sensory fibers containing calcitonin gene related peptide (CGRP) greatly outnumber those with substance P (SP); but both types grow toward the surviving odontoblasts and associated pulp tissue surrounding the lesion. Later during subsequent weeks the nerve fibers accompany granulation tissue as it replaces acute inflammation; and nerve sprouting subsides when inflammation is reduced and when reparative dentin covers the injury site. An important response to tooth injury that may regulate nerve sprouting reactions is the increased production of nerve growth factor (NGF) by pulpal fibroblasts near the lesion. The timing of the nerve sprouting reactions suggests that they may contribute to tooth hypersensitivity after restorative procedures.

Smear layers are created on hard tissues whenever they are cut with hand or rotary instruments. This thin (1-2 microns) layer of denatured cutting debris is very tenacious and, in fact, is often the surface to which restorative materials are luted. The solubility characteristics, chemical reactivity and the structure-function relationships of this layer have not yet been well-defined. During creation of the smear layer, cutting debris is forced variable distances into dentinal tubules. These so-called smear plugs, together with the smear layer decrease dentin permeability, dentin sensitivity and surface wetness. Bonding adhesive resins to smear layers appears to limit the theoretical bond strength unless the smear layers are loosened or partially removed. Future research in this area will include the use of surface analytical techniques such as Auger electron spectroscopy and ESCA. These techniques are required because of the thinness of the smear layer. It is clear that the nature of this critical interface between dental materials and cut hard tissues remains largely unknown. This field will provide fertile ground for future research.

The local regulation of odontoblast response to caries is viewed through initiation and elaboration of sclerotic as well as reparative dentin. Dentin tissue represents a multiple source of potent environment factors when teeth are affected by the demineralization phases of carious process. Some of them have already been identified in sound tissue (matrix glycoproteins, proteoglycans, growth factors, Bone Morphogenetic Protein) and may act on the cell through membrane receptors. Thus, the amplification in collagen synthesis and alkaline phosphatase activity previously observed during sclerotic dentin deposition can be related to the interaction between matrix signals and cell receptors such as the 165 kDa protein shown only by odontoblasts under the affected zone. Similarly, under established lesions generating cell death, the specific matrix made of odontoblasts debris and damage tissues, probably rich in active molecules, may trigger pulp cells to elaborate a cartilage-like layer (identified by type II and XI collagen) followed by odontoblast-like cells to give rise to abnormal tubular dentin. Here, odontoblast response is identical to bone-cells response to injury. What remains to be elucidated concern: The nature of signals found in carious dentin (matrix components, growth factors, bacterial products). The nature and regulation of expression of cell membrane receptors during tooth repair. How the odontoblast produces specific responses to each of these signaling molecules will be the focus of important new investigations.

The use of osteoinductive demineralized dentin matrix in the repair of vital pulp exposures was examined. The pulps of the maxillary first molars of adult male Long Evans rats were exposed and capped with either demineralized dentin particles or guanidinium extracted demineralized dentin particles; then covered with a glass ionomer cement restoration. The animals were sacrificed after two weeks and the maxillae were dissected free, fixed in formaldehyde and demineralized. Histologic examination revealed that in those cases where the protective glass ionomer restoration was intact, both groups showed some healing. There was some preliminary indication that the extent of reactive matrix formation was greater in the osteoinductive group. In both groups, odontoblast-like cells appeared to incorporate some of the dentin particles into the reparative dentin bridge. This preliminary work suggests that osteoinductive factors present in demineralized incisor dentin might be used to guide the formation of a dentin bridge in a rat model for vital pulp exposures.

In hypersensitive teeth pain is typically induced by cold and hot fluids or foods brought to contact with the sensitive dentin or by osmotic and mechanical stimuli. The results of animal experiments indicate that intradental A-type nerve fibres are responsible for the sensitivity of dentin. They are most probably activated by the hydrodynamic mechanism. Thus, their activation is to a great extent dependent on the condition of dentin with either open or blocked dentinal tubules. Blocking of the tubules effectively prevents the nerve activation. Correspondingly, in human experiments, the condition of the dentinal tubules greatly affects dentin sensitivity. In clinical studies significantly more open tubules are found in sensitive compared to non-sensitive areas. However, hypersensitivity may sometimes persist despite of effective blocking of the tubules. This may indicate that some other mechanisms may operate in the nerve activation instead of, or in addition to the hydrodynamic one. Inflammation may sensitize the nerve endings to such an extent that smaller fluid shifts would be sufficient for nerve activation or, for example, thermal stimulation may activate the nerves by a direct effect. On the other hand, spontaneously occurring changes in the exposed dentin, which in many cases seem to block the tubules may reduce the responses to hydrodynamic stimulation and, thus, have an opposite effect on dentin sensitivity. The results of animal experiments indicate that functional changes of this kind may occur. These results also indicate that real dentin hypersensitivity can develop as a result of inflammation induced sensitization of the nerves in the pulp-dentin border in teeth with open dentinal tubules.(ABSTRACT TRUNCATED AT 250 WORDS)

A number of developmental processes can be investigated in the mammalian pulp. Of particular interests are those developmental processes related to when, where and how specific phenotypes are expressed in the forming pulp tissues. This "reaction" attempts to highlight the basic processes related to immunological factors associated with accessory cells, growth factors and the determination and differentiation of odontoblasts, and dentin-specific non-collagenous proteins. The three papers associated with these developmental processes provide an exciting glimpse into the emerging advances being made in pulp biology.