Chapter 1

Synopsis of conservative dentistry

V Gopikrishna

“I keep six honest servingmen (they taught me all I knew); their names are What and Why and When and How and Where and Who...”

— Rudyard Kipling

Definition of conservative dentistry (operative dentistry)

According to Sturdevant, operative dentistry is the art and science of the diagnosis, treatment, and prognosis of defects of teeth that do not require full coverage restorations for correction. It involves the restoration of proper tooth form, function, and aesthetics, while maintaining the physiologic integrity of the teeth in harmonious relationship with the adjacent hard and soft tissues. This field of dentistry is also referred to as conservative dentistry.

Patients seek dental treatment for symptoms, such as pain, sensitivity, trauma, decay, bleeding gums, discolouration of teeth, and for aesthetic corrections. The management of most of these problems is under the purview of this branch of dentistry. Hence, operative dentistry/conservative dentistry forms the core of any dental practice.

Operative dentistry/conservative dentistry deals with:

Indications for conservative dentistry

Structure of teeth and supporting tissues

A tooth has a crown portion seen clinically in the oral cavity and a root portion embedded in a bony socket surrounded by the periodontium (Fig. 1.1).

Fig. 1.1Component tissue and supporting structures of the tooth

Enamel

Dentin

Clinical Note

i. Dentinal tubules adjacent to the pulp → 45,000−65,000/mm²

ii. Dentinal tubules at the DEJ → 15,000−20,000/mm²

○ They form the walls of the pulp cavity.

○ They are avascular, but They are permeable in nature.

Pulp

Pulp is the vital soft connective tissue of the tooth consisting of collagen fibres, vital cells, blood vessels, and nerves. The pulp has four distinct zones (Fig. 1.8):

• Peripheral odontoblastic zone

• Cell-free zone

• Cell-rich zone

• Pulp core

The pulp serves the following functions:

• Formative: Produces both primary and secondary dentin.

• Nutritive: Nutritive supply to odontoblasts.

• Sensory: Transmission of neural impulses.

• Protection: Formation of reparative and sclerotic dentin.

Periodontium

It is the connective tissue structure that attaches the teeth to the maxilla and mandible (Figs 1.9 and 1.10). It consists of:

II. Attachment apparatus

○ Cementum

○ Periodontal ligament

○ Alveolar process

Table 1.1

FDI tooth numbering system

Permanent dentition	Deciduous dentition
FIRST DIGIT	FIRST DIGIT
1 → Maxillary right quadrant	5 → Maxillary right quadrant
2 → Maxillary left quadrant	6 → Maxillary left quadrant
3 → Mandibular left quadrant	7 → Mandibular left quadrant
4 → Mandibular right quadrant	8 → Mandibular right quadrant
SECOND DIGIT	SECOND DIGIT
1 → Central incisor	1 → Central incisor
2 → Lateral incisor	2 → Lateral incisor
3 → Canine	3 → Canine
4 → First premolar	4 → First molar
5 → Second premolar	5 → Second molar
6 → First molar
7 → Second molar
8 → Third molar

Cementum

Dentition

Humans have two sets of teeth: Primary dentition and permanent dentition.

Primary dentition consists of 10 maxillary and 10 mandibular teeth. They are exfoliated and replaced by the permanent dentition, which consists of 16 maxillary and 16 mandibular teeth.

Human teeth are divided into classes on the basis of form and function. Primary dentition has three classes: incisors, canines, and molars. Permanent dentition includes a fourth class, the premolars.

Primary teeth

Permanent teeth

Dental arches and quadrants

Classes of teeth

Cusp: A cusp is an elevation on the crown portion of a tooth making up a divisional part of the occlusal surface.

Ridge: A ridge is any linear elevation on the surface of a tooth and is named according to its location (e.g. buccal ridge, marginal ridge).

Marginal ridges (mesial and distal): These are stress-bearing ridges that border the mesial and distal margins of the occlusal surfaces of posterior teeth as well as the mesial and distal margins of the lingual surfaces of anterior teeth.

Triangular ridges: These are ridges that descend from the tips of the cusps of posterior teeth toward the central part of the occlusal surfaces.

Transverse ridge: It is a ridge formed by the union of a buccal and lingual triangular ridge.

Oblique ridge: It is a ridge that crosses obliquely the occlusal surfaces of maxillary molars and is formed by the union of the traingular ridge of the distobuccal cusp and distal cusp ridge of the mesiolingual cusp.

Fossa: It is an irregular depression or concave area in the enamel surface of a tooth.

Fissure: A developmental linear cleft is usually found at the base of a groove. It is commonly the result of the lack of fusion of the enamel of adjoining dental cusps or lobes (Fig. 1.14b).

Developmental groove: It is a shallow groove or line between the primary parts of a crown or root.

Pit: It is a small pinpoint depression in enamel, usually located in a groove and often at the junction of two or more fissures (Fig. 1.14b).

Tooth surfaces are named according to the anatomical structures it is closest to.

Mesial: Surface toward the midline of the arch.

Distal: Surface away from the midline.

Facial: Surfaces that are in the direction of the cheek or lips.

− Labial: Surface nearer to lip (for an anterior tooth).

− Buccal: Surface nearer to cheek (for posterior tooth).

Lingual: Surface nearer to the tongue (in case of lower teeth).

Palatal: Surface nearer to the palate (upper teeth).

Occlusal: Biting or chewing surface, which contact opposing teeth in occlusion (in posterior teeth).

Incisal: Biting surface of anterior teeth.

Cervical/gingival: Surface nearer to the neck of the tooth or gingival margin.

Proximal: A surface that faces an adjacent tooth.

Interproximal contact: The surface that forms the contact between two adjacent teeth.

Contacts and contours

Knowledge about contacts and contours of various teeth is mandatory for understanding:

• The predisposal factors of proximal caries, like faulty interrelationships.

• Significance of marginal ridges, embrasures, for re-establishing form and function of the restored teeth.

• Periodontal aspect and health of the tooth to be restored.

Ideal contact and contour

Height of contour

• The area of greatest circumference on the facial and lingual surfaces of the tooth is called height of contour (Fig. 1.15).

• It protects the gingival tissue by preventing food impaction.

• In the posterior teeth, the height of contour is located in the gingival third of the facial surface and in the middle one-third of the lingual surface.

Proximal contact area

Proximal contact area denotes the area of proximal height of contour of the mesial or distal surface of a tooth that touches (contacts) its adjacent tooth in the same arch.

Initially, after tooth eruption, there is only one point of contact known as proximal contact point, but due to wear during physiological tooth movement, the proximal contact point becomes proximal contact area.

Location of proximal contact area

• Maxillary and mandibular anteriors → Incisal third and is positioned slightly facial.

• Maxillary and mandibular posteriors → Near the junction of the occlusal and middle thirds or in the middle third.

Embrasures (spillways) (fig. 1.16)

Embrasures are V-shaped spaces that originate at the proximal contact area between the adjacent teeth forming spillway spaces. They are named for the direction toward which they radiate. These embrasures are:

• Facial

• Lingual (Fig. 1.17)

• Incisal or occlusal (Fig. 1.18)

• Gingival (Fig. 1.19)

Normal contour and contact area of the teeth act in deflecting the food only to the extent that the passing food stimulates (by gentle massage) the underlying gingiva (Fig. 1.20).

Under and overcontouring during the restorative treatment has to be avoided as:

Clinical Note

Undercontouring of restorations (fig. 1.21)

a. Trauma to the periodontium

b. Food impaction

Overcontouring of restorations (fig. 1.22)

a. Increased plaque retention

b. Flabby, red, and chronically inflamed gingiva

Figure 1.23 depicts importance of proper contour.

Fig. 1.23Importance of proper contour: Contours. Arrows show pathways of food passing over facial surface of mandibular molar during mastication; (a) Overcontour deflects food from gingiva and results in understimulation of supporting tissues; (b) Undercontour of tooth may result in irritation of soft tissues; (c) Correct contour permits adequate stimulation for supporting tissues, resulting in healthy condition

Occlusion

Occlusion is the relationship of cusps or masticating surfaces of maxillary and mandibular teeth.

Intercuspal position: The position of maximum intercuspation of the teeth.

Occlusal harmony: The absence of occlusal interferences, which allows mandibular movement in all excursions (with the teeth together), and does not result in discomfort, strain, or harm to the teeth or the masticatory apparatus (Fig. 1.24 a, b).

Nomenclature and tooth numbering system

Nomenclature is the scientific way of naming things. It helps in better understanding and communication (Fig. 1.25).

The following are the commonly used tooth notation systems employed by dentists to communicate and record data related to a particular tooth:

I. Zsigmondy—palmer notation system (fig. 1.26)

• Permanent teeth are denoted by numbers 1−8 with central incisor indicated as 1 and progresses on to the third molar which is designated as 8.

• Also called as angular or grid system.

• Deciduous teeth are denoted by upper case English alphabets A to E with A representing central incisor and E representing second molar.

Advantages

Simple to use

Disadvantages

• Not commonly used anymore.

• Each tooth is not denoted by a specific number.

• No differentiation between the same tooth present in the right and left side of the same arch. For example, the nomenclature is the same for both left and right maxillary teeth and so is the case for left and right mandibular teeth.

Permanent teeth

Maxillary right side								Maxillary left side
8	7	6	5	4	3	2	1	1	2	3	4	5	6	7	8
8	7	6	5	4	3	2	1	1	2	3	4	5	6	7	8
Mandibular right side								Mandibular left side

Deciduous teeth

Maxillary right side					Maxillary left side
E	D	C	B	A	A	B	C	D	E
E	D	C	B	A	A	B	C	D	E
Mandibular right side					Mandibular left side

II. Universal notation system or american dental association (ADA) system (fig. 1.27)

• It is also known as Universal system.

• Numbering begins from maxillary right posterior most tooth, which is designated as 1 and proceeds to maxillary left posterior most tooth, which is designated as 16, then to mandibular left posterior tooth, which is designated as 17 and then proceeds to the mandibular right posterior most tooth, which is designated as 32.

• Permanent teeth denoted by number 1−32.

• Deciduous teeth denoted by alphabets A−T.

Permanent teeth

Maxillary right side								Maxillary left side
1	2	3	4	5	6	7	8	9	10	11	12	13	14	15	16
32	31	30	29	28	27	26	25	24	23	22	21	20	19	18	17
Mandibular right side								Mandibular left side

Deciduous teeth

Maxillary right side					Maxillary left side
A	B	C	D	E	F	G	H	I	J
T	S	R	Q	P	O	N	M	L	K
Mandibular right side					Mandibular left side

Advantage

• Separate number/alphabet assigned for each tooth.

Disadvantage

• Confusing and difficult to remember.

III. Federation dentaire international (FDI) system (fig. 1.28)

• Referred as two-digit system, where the two digits are used to identify an individual tooth.

• First digit represents the quadrant (1−4: permanent dentition) (5−8: deciduous dentition)

• Second digit represents the tooth.

Clinical Note

The notation is pronounced individually, i.e. the mandibular left first molar is represented as 36. This has to be pronounced as ‘three six’ and not as ‘thirty six’.

Advantages

• Most commonly employed notation system.

• Each tooth is denoted by a specific number.

• Simple to understand and communicate.

Disadvantages

• Can be confused with ADA numbering system.

• No provision to denote supernumerary tooth.

Permanent teeth

Maxillary right side								Maxillary left side
18	17	16	15	14	13	12	11	21	22	23	24	25	26	27	28
48	47	46	45	44	43	42	41	31	32	33	34	35	36	37	38
Mandibular right side								Mandibular left side

Deciduous teeth

Maxillary right side					Maxillary left side
55	54	53	52	51	61	62	63	64	65
85	84	83	82	81	71	72	73	74	75
Mandibular right side					Mandibular left side

Figure 1.29 depicts both ADA universal and FDI nomenclature systems.

Fig. 1.29 Figure illustrating both the ADA universal nomenclature and FDI nomenclature systems

Causes of loss of tooth structure

The various causes of loss of tooth structure (Fig. 1.30) are provided in Box 1.1.

BOX 1.1

Causes of loss of tooth structure

I. Dental caries

Definition

Dental caries is defined as a multifactorial, transmissible, and infectious oral disease caused primarily by the complex interaction of cariogenic oral flora (biofilm) with fermentable dietary carbohydrates on the tooth surface overtime.

• Dental caries is the most predominant cause of loss of tooth structure (Fig. 1.31).

• It is an irreversible microbial disease of the calcified tissues of the teeth characterized by demineralization of the inorganic portions and dissolution of the organic portion.

Factors causing dental caries (fig. 1.32)

Caries is a multifactorial disease and the most important factors are

• Tooth (host)

• Cariogenic biofilm

• Fermentable carbohydrates

• Time

Pathophysiology of dental caries

Dental plaque or biofilm is a tenaceous film on the surface of teeth composed of bacteria, like Streptococcus sanguis and Streptococcus mutans. These bacteria present in plaque biofilm ferment a suitable dietary carbohydrate substrate to produce acid causing the plaque pH to fall. The critical pH for enamel and dentin is 5.5 and 6.2, respectively. Repeated fall in pH below the critical pH overtime may result in demineralization of a susceptible tooth structure. When the pH returns to neutral and when the concentration of Ca and P supersaturated minerals gets added back to partially demineralized enamel, remineralization starts. This demineralization–remineralization cycle is elaborated in Box 1.2. When the demineralization cycle overwhelms the ability of the host to remineralize, then dental caries manifests clinically.

BOX 1.2

Demineralization and remineralization cycle (From Gopikrishna: Sturdevant’s Art and Science of Operative Dentistry: A South Asian Edition, 2013, Elsevier)

I → Acid production: Cariogenic bacteria in the biofilm metabolize refined carbohydrates for energy and produce organic acid by-products.

II → Critical biofilm pH: These organic acids, if present in the biofilm ecosystem for extended periods, can lower the pH in the biofilm to below a critical level (5.5 for enamel, 6.2 for dentin).

III → Demineralization: The low pH drives calcium and phosphate from the tooth to the biofilm in an attempt to reach equilibrium, hence resulting in a net loss of minerals by the tooth or demineralization.

IV → Remineralization: When the pH in the biofilm returns to neutral and the concentration of soluble calcium and phosphate is supersaturated relative to that in the tooth, mineral can then be added back to partially demineralized enamel, in a process called remineralization.

V → Demineralization and remineralization cycle: This process takes place several times a day over the life of the tooth and is modulated by many factors, including:

VI → Progression of disease: Repeated demineralization events may result from a predominantly pathologic environment causing the localized dissolution and destruction of the calcified dental tissues, evidenced as a caries lesion or a ‘cavity’.

Severe demineralization of enamel results in the formation of a cavitation in the enamel surface.

Subsequent demineralization of the inorganic phase and denaturation and degradation of the organic phase result in dentin cavitation.

The common terms used in this manual to define caries lesions is provided in Box 1.3.

BOX 1.3

Caries lesion—definitions

Caries lesion: Tooth demineralization as a result of the caries process. Other texts may use the term carious lesion. Laypeople may use the term cavity.

Smooth surface caries: A caries lesion on a smooth tooth surface.

Pit-and-fissure caries: A caries lesion on a pit-and-fissure area.

Occlusal caries: A caries lesion on an occlusal surface.

Proximal caries: A caries lesion on a proximal surface.

Enamel caries: A caries lesion in enamel, typically indicating that the lesion has not penetrated into dentin (Note that many lesions are detected clinically, as enamel caries may very well have extended into dentin histologically).

Dentin caries: A caries lesion into dentin.

Coronal caries: A caries lesion in any surface of the anatomic tooth crown.

Root caries: A caries lesion in the root surface.

Primary caries: A caries lesion not adjacent to an existing restoration or crown.

Secondary caries: A caries lesion adjacent to an existing restoration, crown, or sealant. Other term used is caries adjacent to restorations and sealants (CARS). It is also referred to as recurrent caries, which implies that a primary caries lesion was restored, but that the lesion reoccurred.

Residual caries: Refers to carious tissue that was not completely excavated prior to placing a restoration. Sometimes, residual caries can be difficult to differentiate from secondary caries.

Cavitated caries lesion: A caries lesion that results in the breaking of the integrity of the tooth or a cavitation.

Non-cavitated caries lesion: A caries lesion that has not been cavitated. In enamel caries, non-cavitated lesions are also referred to as ‘white spot’ lesions.

(Clinically, the distinction between a cavitated and a non-cavitated caries lesion is not as simple as it may seem. Although historically any roughness detectable with a sharp explorer has been considered a cavitated lesion, more recent caries detection guidelines establish that only lesions in which a blunt probe (e.g. WHO [World Health Organization]/CPI [Communty Periodonatal Index]/PSR [Periodontal Screening and Recording] probe) penetrates are to be considered cavitated. This distinction has important implications on lesion management).

Active caries lesion: A caries lesion that is considered to be biologically active, i.e. lesion in which tooth demineralization is in frank activity at the time of examination.

Inactive caries lesion: A caries lesion that is considered to be biologically inactive at the time of examination, i.e. in which tooth demineralization caused by caries may have happened in the past, but has stopped and is currently stalled. It is also referred to as arrested caries, meaning that the caries process has been arrested, but that the clinical signs of the lesion itself are still present.

Rampant caries: Term used to describe the presence of extensive and multiple cavitated and active caries lesions in the same person. It is typically used in association with ‘baby bottle caries’ or ‘radiation therapy caries’,. These terms refer to the aetiology of the condition.

Classification of dental caries (box 1.4)

I. According to location of caries

The characteristics of a caries lesion vary with the nature of the surface on which the lesion develops.

A. Primary caries

Primary caries is the original caries lesion of the tooth. Three morphologic types of primary caries are evident in clinical observation:

Lesions originating in enamel pits and fissures

Lesions originating on enamel smooth surfaces

Lesions originating on root surfaces.

1. Pit-and-fissure caries

Pits and fissures are particularly susceptible surfaces for caries initiation (Fig. 1.33). The pits and fissures provide excellent mechanical shelter for organisms and harbour a community dominated by S. sanguis and other streptococci. The relative proportion of mutans streptococci (MS) most probably determines the cariogenic potential of the pit-and-fissure community.

Clinical Note

i. The appearance of MS in pits and fissures is usually followed by caries 6−24 months later.

ii. In cross-section, the gross appearance of a pit-and-fissure lesion is an inverted ‘V’ with a narrow entrance and a progressively wider area of involvement closer to the DEJ.

2. Smooth surface caries

The proximal enamel surfaces immediately gingival to the contact area are the second most susceptible areas to caries.

Clinical Note

i. A rough surface (caused by caries, a poor-quality restoration or a structural defect) restricts adequate biofilm removal. This situation favours the occurrence of caries or periodontal disease at this site.

ii. Lesions starting on smooth enamel surfaces have a broad area of origin and a conical or pointed extension toward the DEJ (Fig. 1.34). A cross-section of the enamel portion of a smooth-surface lesion shows a V-shape, with a wide area of origin and the apex of the V directed towards the DEJ.

3. Root surface caries

The proximal, facial, or lingual root surface, particularly near the cementoenamel junction (CEJ), often is unaffected by the action of hygiene procedures, such as flossing, because it may have concave anatomic surface contours (fluting) and occasional roughness at the termination of the enamel. These conditions, when coupled with exposure to the oral environment (as a result of gingival recession), favour the formation of mature and cariogenic biofilm and proximal root surface caries (Fig. 1.35).

BOX 1.4

Classification of dental caries

Clinical Note

B. Secondary (recurrent) caries

Secondary caries occurs at the junction of a restoration and the tooth and may progress under the restoration. It is often termed recurrent caries. This condition usually indicates that microleakage is present, along with other conditions conducive to caries development.

II. According to direction of caries

A. Backward caries

When the spread of caries along the DEJ exceeds the caries in the contiguous enamel, caries extends into this enamel from the junction and is termed backward caries (Fig. 1.36).

Fig. 1.36Forward decay/caries and backward caries

B. Forward caries

Forward caries is said to be present, wherever the caries in enamel is larger or at least the same size as that in dentin (Fig. 1.36).

III: According to extent of caries

A. Incipient caries/white spot lesion (reversible)

Incipient caries or white spot lesion (WSL) is the first evidence of caries activity in enamel. On smooth surface enamel, the lesion appears opaque white when air-dried and seems to disappear when wet (Fig. 1.37).

Fig. 1.37White spot lesions (WSL) at the cervical margins of teeth

Clinical Note

i. This lesion may be characterized as reversible and the enamel surface is fairly hard, intact, and smooth to touch.

ii. The lesion can be remineralized, if immediate corrective measures alter the oral environment, including plaque removal and control.

iii. A remineralized lesion usually is either opaque white or a shade of brown-to-black from extrinsic colouration, has a hard surface, and appears the same whether wet or dry.

B. Cavitated caries (irreversible)

In cavitated caries, the enamel surface is broken (not intact) and usually the lesion has advanced into dentin. Usually, remineralization is not possible and treatment that includes tooth preparation and restoration is indicated (Fig. 1.38).

IV. According to rate (speed) of caries

A. Acute (rampant) caries

Acute caries, often termed rampant caries, refers to disease that rapidly damages the tooth. It is usually in the form of numerous soft, lighter-coloured lesions in a mouth and is infectious (Fig. 1.39A).

B. Chronic (slow) or arrested caries

Chronic caries is slow or it may be arrested after several active phases. The slow rate results from periods, when demineralized tooth structure is almost remineralized (the disease is episodic overtime, because of changes in the oral environment). The condition may be found in only a few locations in a mouth and the lesion is discoloured and fairly hard (Fig. 1.39B).

Clinical Note

i. The slow rate of caries allows time for extrinsic pigmentation and an arrested enamel lesion is brown-to-black in colour.

ii. An arrested caries lesion is hard, as a result of fluoride and may be more caries-resistant than contiguous, unaffected enamel.

iii. An arrested dentinal lesion typically is open (allowing debridement from tooth brushing), dark and hard, and this dentin is termed eburnated dentin.

V. According to the histological depth of penetration

A. Enamel caries

i. Non-cavitated enamel caries or incipient caries (white spot lesion)

The earliest evidence of caries on the smooth enamel surface of a clean, dry tooth is seen as a white spot. White spots are chalky white, opaque areas (Fig. 1.40) that are revealed only when the tooth surface is desiccated and are termed non-cavitated enamel caries lesions or incipient caries or white spot lesions (WSL). These areas of enamel lose their translucency, because of the extensive subsurface porosity caused by demineralization. However, it has also been shown experimentally and clinically that non-cavitated caries of enamel can remineralize (Box 1.5).

Fig. 1.40Incipient caries or white spot lesion (WSL)

BOX 1.5

Remineralization mechanism of a white spot lesion (WSL)

The supersaturation of saliva with calcium and phosphate ions serves as the driving force for the remineralization process

Non-cavitated enamel lesions retain most of the original crystalline framework of the enamel rods, and the etched crystallites serve as nucleating agents for remineralization

Calcium and phosphate ions from saliva can penetrate the enamel surface and precipitate on the highly reactive crystalline surfaces in the enamel lesion

The presence of trace amounts of fluoride ions during this remineralization process greatly enhances the precipitation of calcium and phosphate, resulting in the remineralized enamel becoming more resistant to subsequent caries attack, because of the incorporation of more acid-resistant fluorapatite

Remineralized (arrested) lesions can be observed clinically as intact, but discoloured, usually brown or black, spots. The change in colour is presumably caused by trapped organic debris and metallic ions within the enamel. These discoloured and remineralized arrested caries areas are intact and are more resistant to subsequent caries attack than the adjacent unaffected enamel. They should not be restored, unless they are aesthetically objectionable.

Location: These lesions usually are observed on the facial and lingual surfaces of teeth. They can also occur in the proximal surfaces, but are difficult to detect.

Remineralization mechanism

The remineralization mechanism of white spot lesion (WSL) is summarized in Box 1.5.

Clinical Note

i. Care must be exercised in distinguishing white spots of non-cavitated caries from developmental white spot hypocalcifications of enamel.

ii. Non-cavitated (white spot) caries partially or totally disappears visually when the enamel is hydrated (wet), whereas hypocalcified enamel is affected less by drying and wetting.

iii. Hypocalcified enamel does not represent a clinical problem, except for its aesthetically objectionable appearance.

iv. Injudicious use of an explorer tip can cause actual cavitation in a previously non-cavitated area, requiring in most cases, restorative intervention.

v. Role of explorer the recommended instrument for probing is CPITN probe having a 0.5 mm ball-ended tip. Probing should be done judiciously with tactile sensation to detect surface roughness, by gently stroking across the tooth surface (Fig. 1. 41).

ii. Cavitated enamel caries

Cavitated enamel lesions can be initially detected as subtle breakdown of the enamel surface. These lesions are very sensitive to probing and can be easily enlarged by using sharp explorers and excessive probing force. More advanced cavitated enamel lesions are more obviously detected as enamel breakdown.

Clinical Note

This stage cannot be remineralized and the carious lesion has to be removed and the tooth restored with an appropriate restoration.

Zones of enamel caries

The four zones in a sectioned incipient lesion when examined in quinoline by transmitted light are:

1. Translucent zone.

2. Dark zone.

3. Body of the lesion.

4. Surface zone.

B. Dentin caries

Progression of dental caries (Fig. 1.42)

Rate of progression: Caries advances more rapidly in dentin than in enamel because:

Dentin provides much less resistance to acid attack owing to less mineralized content.

Dentin possesses microscopic tubules that provide a pathway for the ingress of bacteria and egress of minerals

Shape of lesion: Dentin caries is V-shaped in cross-section with a wide base at the DEJ and the apex directed pulpally (Figs 1.43 and 1.44).

Fig. 1.43Progression of caries in pits and fissures. (a) The initial lesions develop on the lateral walls of the fissure. Demineralization follows the direction of the enamel rods, spreading laterally as it approaches the DEJ; (b) Soon after the initial enamel lesion occurs, a reaction can be seen in the dentin and pulp. Forceful probing of the lesion at this stage can result in damage to the weakened porous enamel and accelerate the progression of the lesion; (c) Initial cavitation of the opposing walls of the fissure cannot be seen on the occlusal surface; (d) Extensive cavitation of the dentin and undermining of the covering enamel will darken the occlusal surface

Clinical Note

i. All proximal surfaces are demineralized to some degree, but most are remineralized and become immune to further attack.

ii. An intact surface is essential for successful remineralization and arrest of the lesion.

iii. The use of a sharp explorer to detect cavitation is problematic, because excessive force in application of the explorer tip during inspection of the proximal surfaces can damage weakened enamel and accelerate the caries process by creating cavitation.

iv. Cavitation is an irreversible process and requires restorative treatment/correction of the damaged tooth surface.

Dentinal reaction to caries

The three levels of dentinal reaction to caries that can be recognized are:

Reaction to a long-term, low-level acid demineralization associated with a slowly advancing lesion → Sclerotic dentin formation

Reaction to a moderate-intensity attack → Reparative dentin formation

Reaction to severe, rapidly advancing caries characterized by very high acid levels → Pulpal necrosis and periradicular progression of disease

I. Reaction to a long-term, low-level acid demineralization associated with a slowly advancing lesion: Sclerotic dentin formation

Dentin that has more mineral content than normal dentin is termed sclerotic dentin.

Sclerotic dentin formation occurs ahead of the demineralization front of a slowly advancing lesion and may be seen under an old restoration.

Sclerotic dentin is usually shiny and darker in colour, but feels hard to the explorer tip. By contrast, normal freshly cut dentin lacks a shiny, reflective surface and allows some penetration from a sharp explorer tip.

The apparent function of sclerotic dentin is to wall off a lesion by blocking (sealing) the tubules.

II. Reaction to a moderate-intensity attack: Reparative dentin formation

The second level of dentinal response is to moderate-intensity irritants, by forming reparative dentin (Box 1.6).

BOX 1.6

Mechanism of reparative dentin formation

Infected dentin contains a wide variety of pathogenic materials or irritants, including high acid levels, hydrolytic enzymes, bacteria, and bacterial cellular debris.

The pulp may be irritated sufficiently from high acid levels or bacterial enzyme production to cause the formation (from undifferentiated mesenchymal cells) of replacement odontoblasts (secondary odontoblasts)

These cells produce reparative dentin (reactionary dentin) on the affected portion of the pulp chamber wall

III: Reaction to severe, rapidly advancing caries characterized by very high acid levels: Pulpal necrosis and periradicular progression of disease

The third level of dentinal response is to severe irritation. Acute, rapidly advancing caries with high levels of acid production overpowers dentinal defences and results in infection, abscess, and death of the pulp (Box 1.7).

BOX 1.7

Mechanism of pulpal necrosis

Small, localized infections in the pulp produce an inflammatory response involving capillary dilation, local oedema, and stagnation of blood flow

As the pulp is contained in a sealed chamber, and its blood is supplied through narrow root canals, any stagnation of blood flow can result in local anoxia and necrosis

The local necrosis leads to more inflammation, oedema, and stagnation of blood flow in the immediately adjacent pulp tissue, which becomes necrotic in a cascading process that rapidly spreads to cause entire pulpal necrosis

Clinical Note

i. Maintenance of pulp vitality depends on the adequacy of pulpal blood supply.

ii. Recently erupted teeth with large pulp chambers and short, wide canals with large apical foramina have a much more favourable prognosis for surviving pulpal inflammation, than fully formed teeth with small pulp chambers and small apical foramina.

Zones of dentin caries

Three different zones have been described in carious dentin (Fig. 1.45).

Fig. 1.45Dentinal caries with outer infected dentin and inner affected dentin

Zone 1: Normal dentin

• The deepest area is normal dentin, which has tubules with odontoblastic processes that are smooth and no crystals are present in the lumens.

• The intertubular dentin has normal cross-banded collagen and normal dense apatite crystals.

• No bacteria are present in the tubules.

• Stimulation of dentin (e.g. by osmotic gradient [from applied sucrose or salt], a bur, a dragging instrument, or by desiccation from heat or air) produces a sharp pain.

Zone 2: Affected dentin

• Also called inner carious dentin, affected dentin is a zone of demineralization of intertubular dentin and of initial for mation of fine crystals in the tubule lumen at the advancing front.

• Damage to the odontoblastic process is evident.

• Affected dentin is softer than normal dentin and shows loss of mineral from intertubular dentin and many large crystals in the lumen of the dentinal tubules.

• Stimulation of affected dentin produces pain.

• Although organic acids attack the mineral and organic contents of dentin, the collagen cross-linking remains intact in this zone.

• The intact collagen can serve as a template for remineralization of intertubular dentin and this region remains capable of self-repair, provided that the pulp remains vital.

• The affected dentin zone can also be subclassified into three subzones:

a. Subtransparent dentin

b. Transparent dentin

c. Turbid dentin

Zone 3: Infected dentin

Clinical Note

i. In operative procedures, it is convenient to term dentin as either infected, which requires removal, or affected, which does not require removal.

ii. To clinically distinguish these two layers, the operator traditionally observes the degree of discolouration (extrinsic staining) and tests the area for hardness by the feel of an explorer tine or a slowly revolving bur. Some difficulties occur with this approach, because:

- The discolouration may be slight and gradually changeable in acute (rapid) caries.

- The hardness (softness) felt by the hand through an instrument may be an inexact guide.

iii. To differentiate between remineralizable and non-remineralizable dentin, staining carious dentin was proposed by Fusayama. The outer layer (infected dentin) can be selectively stained in vivo by caries detection solutions, such as 1% acid red 52 (acid rhodamine B or food red 106) in propylene glycol. This solution stains the irreversibly denatured collagen in the outer carious layer, but not the reversibly denatured collagen in the inner carious layer. Clinical use of this staining technique may provide a more conservative tooth preparation, because the boundary between the two layers differentiated by this technique cannot easily be detected in a tactile manner.

iv. When sclerotic dentin is encountered, it represents the ideal final excavation depth; because, it is a natural barrier that blocks the penetration of toxins and acids.

Visual clinical examination using international caries detection and assessment system (ICDAS)

The ICDAS was developed to serve as a guide for standardized visual caries assessment that could be used for clinical practice, clinical research, education, and epidemiology. During the clinical examination, every accessible surface of each tooth must be inspected for localized changes in colour, texture, and translucency, as described in the ICDAS codes.

Preliminary preparation

This requires two minimum conditions for the examination to be properly conducted:

- Biofilm or plaque must be thoroughly removed from teeth prior to the examination.

- Teeth must be sufficiently air-dried, so that the changes can be seen properly.

The visual examination is then conducted in a dry, well-illuminated field. Through direct vision and reflecting light through the occlusal surface of the tooth, the occlusal surface is diagnosed as diseased, if chalkiness or apparent softening or cavitation of tooth structure forming the fissure or pit is seen or a brown-gray discolouration, radiating peripherally from the fissure or pit, is present.

ICDAS assessment

The ICDAS uses a two-stage process to record the status of the caries lesion. The first is a code for the restorative status of the tooth and the second is for the severity of the caries lesion. The status of the caries severity is determined visually on a scale 0−6:

This severity code is paired with a restorative/sealant code 0−8:

See Figure 1.46 for the ICDAS for examples of coding for restorative status and caries severity. The details of this system for detection and training to use the system with an online tutorial are available at www.icdas.org.

Fig. 1.46*International Caries Detection and Assessment System (ICDAS)* chart showing visual caries detection. Source: (From Gopikrishna: Sturdevant’s Art and Science of Operative Dentistry: A South Asian Edition, 2013, Elsevier)

Non-carious destruction of tooth

I. Tooth wear

II. Trauma

III. Developmental defects

I. Tooth wear

1. Attrition

• Loss of tooth structure on chewing surfaces (occlusal and incisal) is due to frictional forces between contacting surfaces (Fig. 1.47).

• It is physiological and age-dependent.

BOX 1.8

Developmental defects of teeth

Acquired development defects	Hereditary conditions
1. Enamel hypoplasia (Fig. 1.52) Fig. 1.52Enamel hypoplasia	1. Hypodontia/microdontia
2. Dental fluorosis (Fig. 1.53) Fig. 1.53Fluorosis	2. Amelogenesis imperfecta (Fig. 1.55) Fig. 1.55 Amelogenesis imperfecta
3. Tetracycline staining (Fig. 1.54) Fig. 1.54Tetacycline staining of the teeth	3. Dentinogenesis imperfecta (Fig. 1.56) Fig. 1.56Dentinogenesis imperfecta