A: Early detection of fissure caries is a prerequisite for effective management. Clinical decisions regarding the type of agent most appropriate for the prevention and chemotherapeutic treatment of root caries depend primarily on the professional assessment of risk for the lesions (Anusavice, 1995).

For approximal tooth surfaces, the results of several in-vivo studies were reviewed (Ismail 1997). The study evaluated the diagnosis of different stages of dental caries in the proximal surface area and found precavitated lesions to be the most common. Probing was found to be the least effective method for the detection of carious lesions. The FOTI exhibited a better sensitivity than clinical inspection in detecting precavitated lesions that had a shadow or opacity underneath the marginal ridge.

Another study (Van Rijkom and Verdonschot 1995) also reviewed the diagnosis of caries on proximal surfaces and found that FOTI was superior to visual inspection and radiography. However in a previous review (Verdonschot 1991) radiography was superior to FOTI. A conclusion can be obtained from some of the previous studies that FOTI is a cost efficient non-invasive adjunct to a clinical examination in the detection of posterior dental caries (Pine CM 1996).

In a statement issued by the National Institutes of Health Consensus Development Conference(2001) on the diagnosis of caries, each of these detection methods were reviewed by an independent, non-Federal Consensus Development Panel. After weighing the scientific evidence, the panel’s draft statement concluded that the differences in caries presentations and behavior in different anatomical sites makes it unlikely that any one diagnostic modality will have adequate sensitivity and specificity of detection for all sites.

Existing diagnostic modalities appear to have satisfactory sensitivity and specificity in diagnosing substantial, cavitated, dental caries; specifically radiographic methods are essential in diagnosing approximal carious lesions. However, these modalities do not appear to have sufficient sensitivity or specificity to efficaciously diagnose noncavitating caries, root caries, or secondary caries. Currently, there is no diagnostic modality that can differentiate between microbiologically active caries and demineralized dentin without caries activity beneath a restoration. This is a critical weakness in view of the significant percentage of restorations inserted to replace existing restorations.

The need for the identification and clinical staging of the presence, activity, and severity of dental caries is of paramount importance in the deployment of treatment strategies that employ increasingly important nonsurgical modalities, such as fluoride, antimicrobials, sealants, and no treatment. New diagnostic modalities that are currently in various stages of development and testing will need to be evaluated using rigorously controlled clinical trials. Such studies will promote true staging of carious lesions, based on highly sensitive and specific diagnoses, followed by appropriate, linked, treatment-planning decision algorithms.

A review conducted by Dodds (1993) on the effective application of various diagnostic systems were tabulated as follows: The Relative Utility of the Available Diagnostic Systems in Diagnosing Early Noncavitated Lesions.

Clinical observations suggest that carious lesions can be arrested at any stage of lesion development i.e., even at the cavitation stage if plaque-free conditions are maintained (Nyvad and Fejerskov, 1997). The remineralization observed in clinically arrested lesions and the conversion of clinically active to inactive lesions supports the non-restorative management of carious lesions (Nyvad and Fejerskov, 1986). Therefore, sensitive diagnostic techniques are needed to provide acceptable compromises between sensitivity and specificity for a wide range of applications for individual patient care as well as for research purposes.

However, existing diagnostic techniques generally rely on subjective judgements and can only provide semi-quantitative measures and some of the diagnostic systems are unable to detect small lesions. The ECM is capable of detecting PFCLs, which may be missed with conventional visual examination.

A: Enamel is a secretion rather than a true tissue because no viable ameloblasts exist after the eruption of the teeth. Caries, a disease of mineralized tissues, is caused by the action of micro-organisms on fermentable carbohydrates in the diet, which cause demineralization of the mineral portion of these tissues. This is followed by disintegration of organic material. (Thylstrup and Fejerskov, 1994). The classic causal prescription for dental caries includes these three factors.

In human cross-sectional epidimiological studies, S. mutans has been correlated with caries and presumed to play a major role in the initiation of the lesion, although it is not the first to colonize the tooth surface (Loesche et al., 1975). Lactobacilli have also been correlated with dental caries. However, these species are minimally involved in the initiation of the lesion but play a major role in the progression of it.

Millar (1890) postulated the theory of multiple bacteria-causing caries rather than a single group, a theory supported by others to date. When comparing the microbial composition of dental plaque from persons with low caries activity with those having high caries activity, the number of acidogenic bacteria was greater in the latter group.

Cariogenic bacteria utilize sugar (by possessing special enzymes) in its metabolism. The resultant energy is used to produce special intracellular and extracellular glucans (polymers) that help it populate and grow in large numbers or masses. The formation of these masses is important for the initiation of the carious process.

Fermentation of the carbohydrates in these anaerobic conditions causes an increase in the concentration of organic acids, mainly lactic acid, in the plaque and in the carious lesion. The resulting drop in pH causes demineralization while the acid-free periods in the absence of carbohydrates (resting periods) have no demineralization activity. The balance against those continuous attacks is a function of multiple complex factors. The content of the food intake, plaque quantity and quality, the quantity and quality of saliva, the susceptibility of the tooth surface, and fluoride concentration in the environment are among the important factors that interact with each other to produce caries or inhibit caries. This is one of the reasons for the importance of controlling the intake of fermentable carbohydrates in the diet.

Caries is an etiologically complex disease process. It is likely that numerous microbial, genetic, immunological, behavioral, and environmental contributors to risk are at play in determining the occurrence and severity of clinical disease. Assessment tools based on a single risk indicator are therefore unlikely to accurately discriminate between those at high and low risk. Multiple indicators, combined on an appropriate scale and accounting for possible interactions, will certainly be required.

A: Dental caries produces its effects locally by spreading in the mineralized tissue with no symptoms. Once the process reaches the vital pulp then pain may be felt from sensitivity to cold or osmotic stimuli from foods. If the decay is left to progress, then an infection is established in the pulp chamber and spontaneous pain is produced. The immune response usually can contain the bacteria within the pulp chamber, but a fistula may be established between the tooth apex and the oral cavity, which drains pus.

Systemic effects of the caries process can occur when the infection is not drained. The building pressure of the infection and bacterial products spread internally within the adjacent tissue, and a swelling can be produced in the facial tissue surrounding the offensive tooth. This might be associated with fever, malaise, and in some cases erythema of the skin. A further serious complication appears when the infection reaches critical areas such as around the eye or down to the neck that might endanger the air passageways or risk a brain infection. In cases where the immunity is reduced by drugs or disease, the total body spread of infection is called septicaemia and risks the life of the patient.