Further reading and references
2.3.5 The shape of the lesion and its clinical implication
On a smooth surface the lesion is classically triangular in shape. It follows the direction of the enamel prisms and can be thought of as multiple individual lesions each at a different stage of progression. The central traverse, where the lesion is deepest, is the oldest and most advanced part of the lesion where the biofilm is thickest. The shape of the lesion and the activity of the lesion entirely reflect the specific environmental conditions of the overlying biofilm (Figure 2.5).
Occlusally, purely because of the sloping fissure walls and the direction of the enamel prisms, the lesion assumes an undermining character. This explains why in the more advanced lesion, where there appears to be a small hole in the tooth, something apparently so small on the surface can be so large when entered with a burr (Figure 2.9) Once a cavity forms on this surface it is rather like a Marmite pot, narrower at the top than at the base (Figure 2.10). Now the toothbrush cannot reach into the hole to remove the plaque and the lesion is bound to progress.
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Figure 2.10. A hemisected occlusal lesion where there is a cavity in the tooth down to the dentine. At this stage the lesion spreads laterally along the enamel- dentine junction. Notice the shape of the cavity. It is wider at the base than at the top. This would prevent the patient cleaning plaque out of the hole.
2 . 4 D E N T I N E R E A C T I O N S
The dentine has been reacting to the carious process in the biofilm long before a cavity forms. Dentine is a vital tissue, permeated by the tubules containing the cell processes of the odontoblasts, and it defends itself by the tubular sclerosiswithin the dentine and the formation of tertiary dentine (also called reactionary dentine or reparative dentine) at the pulp-dentine border (Figure 2.11).
Tubular sclerosis is the deposition of mineral within the dentinal tubules and it requires the presence of a vital odontoblast. It can be seen in the light microscope where a traverse through the centre of the enamel lesion crosses the enamel–dentine junction. The enamel demineralization has increased the enamel porosity and permeability and this dentine reac- tion corresponds to the most porous part of the enamel lesion, which in turn corresponds to the activity of the biofilm (Figure 2.12).
When contact between the enamel lesion and the enamel–dentine junc- tion is established, the first sign of dentine demineralization can be seen along the junction as a brownish discolouration within the contact area of the enamel lesion and the junction. Demineralization of outer dentine is now surrounded by sclerotic reactions corresponding to the less advanced peripheral parts of the enamel lesion. Once again the dentinal changes merely represent a continuum of pulpodentinal reactions to the activity of the biofilm and transmission of the stimulus through the enamel in the direction of the enamel prisms. This means that regular disturbance or removal of the biofilm will arrest the progression of lesions, but the deminer- alized dentine remains as a scar in the tissue. It is very important to realize
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Figure 2.11. A ground section of a molar crown viewed in transmitted light.
A fissure lesion is present. The enamel is cavitated. Tubular sclerosis is seen as a translucent zone in the dentine (TZ). Reactionary dentine (RD) is also present since the pulp horn is partially obliterated. (By courtesy of Professor N. W.
Johnson.)
that this dentine involvement per seis not an indicator for operative treat- ment. This dentine involvement is not actually an important moment clini- cally, but part of a continuum of changes all driven by the biofilm at the tooth surface.
2 . 5 C A V I T A T I O N — A N I M P O R T A N T M O M E N T C L I N I C A L LY
The important moment clinically may be the breakdown of the outer ena- mel, presumably created by mechanical injuries during mastication, micro- traumas during interdental wear, or careless probing. It is important because now it may be difficult to clean the biofilm out of the cavity (Figure 2.10).
This protected area results in an ecological shift towards anaerobic and acid- producing bacteria. Once the biofilm is sitting on the dentine, demineraliza- tion can spread laterally along the enamel–dentine junction, undermining sound enamel (Figure 2.13).
C L I N I C A L A N D H I S TO L O G I C A L F E AT U R E S O F C A R I O U S L E S I O N S 3 1
S Body TZ DZ Dead tract
Normal
Translucent zone
Reactionary dentine
Figure 2.12. Diagram of histological changes in enamel and dentine before cavitation of the enamel.
S, Surface zone; Body, body of lesion; DZ, dark zone; TZ, translucent zone.
(By courtesy of Professor N. W. Johnson.)
Destruction Penetration Demin.
Reactionary
Body TZ
Normal +
Figure 2.13. Diagram of histological changes after cavitation. Note that demineralization of enamel precedes bacterial penetration.
TZ, translucent zone;
DEMIN, demineralization.
(By courtesy of Professor N. W. Johnson.)
2 . 6 D E N T I N E C H A N G E S I N T H E C A V I T A T E D L E S I O N : D E S T R U C T I O N A N D D E F E N C E
Following exposure of dentine to the mass of bacteria in the cavity, the most superficial part of the dentine is decomposed by the action of acids and proteolytic microorganisms. This is known as the zone of destruction.
Beneath this, tubular invasion of bacteria is frequently seen which is called thezone of penetrationbecause the tubules have become penetrated by microorganisms. Beyond this is an area of demineralized dentinewhich does not yet contain bacteria (Figure 2.13). When lesions progress rapidly, so-calleddead tractsmay form. Here the odontoblast processes have been destroyed without producing tubular sclerosis.
These tubules are invaded by bacteria and groups of tubules coalesce forming liquefaction foci (Figure 2.14). Destruction may also advance along the incremental lines of growth which are at right angles to the tubules to produce transverse clefts(Figure 2.15).
The defence reactions of tubular sclerosis and tertiary dentine formation continue as a response to these destructive processes. Both processes reduce the permeability of the dentine, although tertiary dentine is less well miner- alized than primary or secondary dentine and contains irregular dentinal tubules. Even at this late stage removal of the mass of bacteria in the cavity, and/or placing a seal so the patient can clean, arrests the progression of
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Figure 2.14. Decalcified section of carious dentine showing dentinal tubules penetrated by deeply staining bacteria. In places the tubules appear to have been pushed apart by aggregations of bacteria called liquefaction foci. (By courtesy of Professor N. W. Johnson.)
lesions and encourages the two reparative processes. Even when dead tracts have formed and odontoblasts have been destroyed, new odontoblasts can form from fibroblasts in the pulp and lay down dentine. This is called repara- tive dentine. If the destructive processes continue, eventually the pulp becomes inflamed.
2 . 7 I N F L A M M A T I O N O F T H E P U L P
Inflammation is the fundamental response of all vascular connective tissues to injury. Inflammation of the pulp is called pulpitisand, as in any other tissue, it may be acute or chronic. The duration and intensity of the stimulus is partly responsible for the type of response. A low-grade, long-lasting stim- ulus may result in chronic inflammation whereas a sudden, severe stimulus is more likely to provoke an acute pulpitis.
In a slowly progressing carious lesion in dentine, the stimuli reaching the pulp are bacterial toxins and thermal and osmotic shocks from the external environment. The response to these low-grade, sustained stimuli is chronic inflammation which is well localized beneath the cavity. One rationale for restoring a cavity in a tooth is to remove or seal in the soft, infected dentine which is acting as an irritant, and fill the cavity with a restoration. The local inflammation then has the potential to repair. However, if the carious process continues, the organisms actually reach the pulp to create a ‘carious expo- sure’, and now localized acute inflammation is likely to be superimposed on the chromic inflammation.
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Figure 2.15. Decalcified section of carious dentine showing tubules penetrated by bacteria. The tissue appears to have split at right angles to the tubules along the incremental lines of growth. These splits are called transverse clefts.
(By courtesy of Professor N. W. Johnson.)
Inflammatory reactions have vascular and cellular components. The cel- lular component is most obvious in chronic inflammation (Figure 2.16) with lymphocytes, plasma cells, monocytes, and macrophages all present within the tissue. In time there may be increased collagen production leading to fibrosis. These chronic inflammatory reactions may not endanger the vitality of the tooth.
Unfortunately, the same cannot be said of acute inflammation, since in this process the vascular changes predominate, including dilation of blood vessels, producing an initial acceleration of blood flow and fluid exudate.
This exudate may later result in retardation of blood flow and vascular stasis.
There is active emigration of neutrophils (Figure 2.17) and all these factors contribute to an increase in tension of the tissue.
The outcome of this process is often localized necrosis, and in time this may involve the entire pulp. The sequel to pulpal necrosis is spread of inflammation into the periapical tissues (apical periodontitis). Once again, the inflammatory response may be acute or chronic.