Caries, pulpitis & periapical lesions

: 07-3121101~2755 yukkwa@kmu.edu.tw

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DENTAL CARIES
Etiology Epidemiology Clinical Types Enamel Caries Dentin Caries

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PULPITIS
Reversible Pulpitis Irreversible Pulpitis Pulp Necrosis

Common Diagnostic Techniques

History and Nature of Pain Reaction to Thermal Changes Reaction to Electric Stimulation Reaction to Percussion of tooth Radiographic Examination Visual Examination Palpation of Surrounding Area
Histopathology of Pulpal Diseases

Acute Pulpitis Chronic Pulpitis Chronic Hyperplastic Pulpitis

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Periapical Lesions Chronic Apical Periodontitis Periapical Granuloma Periapical Cyst Acute Periapical Conditions Periapical Abscess

References
1. Sapp JP: Contemporary Oral & Maxillofacial Surgery, p. 61-87 2. Matalon S et al. Detection of cavitated carious lesions in approximal tooth surfaces by ultrasonic caries detector. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;103:109-13 3. http://www.ne.jp/asahi/fumi/dental/ 4. www.teethwhiteningkits.com/tooth_decay/t5_tooth_decay_children.htm 5. www.odonto-red.com/cariesdental.htm 6. www.lezerdent.hu/cariesn.htm 7. www.areadent.cl/ 8. www.kavo.com/Es 9. www.uic.edu/classes/dh/dh110/Caries_files 10. http://iwate8020.jp/know/caries.html 11. http://www.suwaneedental.com/cariesprevention.htm 12. http://www.drfarid.com/fluoride.htm

Etiology
It is a multifaceted disease involving an interplay among the teeth, oral host factors of saliva, microflora, and external factors of diet. It is a unique form of infection with acidic and proteolytic bacteria for enamel caries

Etiology

Refs. 3, 4

Etiology

Refs. 1, 3

Etiology

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Refs. 4, 6

Etiology

Refs. 10, 11

Etiology
The Caries Balance
Pathological Factors
Acidogenic bacteria [mutans Streptococci] Reduced salivary function Frequency of fermentable carbohydrate ingestion

Protective Factors
Saliva flow & components Proteins, calcium phosphate fluoride, immunoglobulins in saliva Extrinsic chlorhexidine

Caries

No Caries

Saliva - contains materials for remineralization - calcium and phosphate ions

Healthy tooth enamel rods Enamel rods demineralized ( broken down by acid) Enamel rods remineralized, rebuilt, by fluoride & minerals in saliva

Refs. 5, 12

Epidemiology
 1 of common chronic diseases in the world  Prevalence - increased in modern times  Increase associated with dietary changes  Trend beginning to decline in some countries y(i.e. certain segments of US, Western Europe, yNew Zealand, and Australia) Cause of decline? It is attributed to fluoride
DENTAL PLAQUE = gelatinous mass of bacteria
Ref. 5

Clinical Types
 Pit and fissure

 Smooth surface  Cemental  Recurrent

Clinical Types (1)

Pit and fissure caries : the most common type : appear at an early age : on the occlusal & buccal surfaces of the molars

Refs. 1, 4

Clinical Types (2)

Ref. 6

Clinical Types (3)

Ref. 8

Clinical Types (4)

Ref. 8

Clinical Types (5)

Ultrasonic caries detector

Ref. 2

Clinical Types (6)

Smooth surface : less common caries : occurs on the labial surface & proximal area

Ref. 1

Clinical Types (7)

Refs. 1, 6

Clinical Types (8)

Cemental (root) caries 1. Found in older people, especially, gingival recession 2. Progress differently than enamel & dentin caries because root surfaces are soft, thin, and subject to chemical erosion and abrasive action during tooth brushing 3. Both acid and enzyme producing bacteria and thin layer of dentin results in rapid progression into pulp

Ref. 1

Clinical Types (9)

Recurrent caries arises around an existing restoration as a result of marginal leakage. Marginal leakage is a situation predispose the tooth to accumulate bacteria and food.

Clinical Types (10)

Acute (rampant) caries and chronic caries are infrequently used terms to denote the rate that dental caries progresses in patients

Ref. 4

Enamel Caries (1)

Smooth surface enamel caries is most commonly located on the mesial and distal surfaces at the point of contact with the adjacent tooth (interproximal caries). The less common lesions on the buccal and lingual surfaces

Arrested form - chalky appearance Advanced form - Cavitation

Ref. 1

Enamel Caries (2)

Hypocalcified enamel - structure is abnormal - not weakened, surface is hard Incipient caries - porous weakened structure - surface is softened Arrested caries (remineralized) - strong, surface is hard Active caries - cavitated, weak enamel, surface is soft

Ref. 1

Enamel Caries (3) Hypocalcified enamel restore only for esthetics yIncipient caries y anti-microbial (remineralization) y restore (after remineralization) y only for esthetics yArrested caries (remineralized) y restore only for esthetics Active caries  anti-microbial + restorative

Enamel Caries (4)

Histopathology Four zones on ground section
1. 2. 3. 4. Translucent zone: advancing front of initial demineralization Dark zone: remineralization Body of lesion: region of maximal demineralization Surface zone: remain unaffected until it is collapsed forming a cavity

Surface zone Body of lesion Dark zone

Translucent zone

Enamel
Ref. 1

Enamel Caries (5)

Incipient Lesion - 4 Zones Zone 1 - translucent zone Zone 2 - dark zone Zone 3 - body of the lesion Zone 4 - surface zone

B
lesion = cone shaped

SZ

Ref. 9

body of lesion (B) appears dark beneath relatively INTACT SURFACE ZONE

Enamel Caries (6)

Incipient Lesion - 4 Zones Zone 1 - translucent zone Zone 2 - dark zone Zone 3 - body of the lesion Zone 4 - surface zone

TZ DZ

Ref. 9

TRANSLUCENT ZONE (TZ) present at advancing front of lesion DARK ZONE superficial to TZ

Enamel Caries (7)

Zone 1 - translucent zone 1. deepest zone - closest to pulp 2. advancing front of lesion 3. appears structureless - (polarized light) 4. pore volume - 1% - > 10v normal enamel 5. pores/voids form along prism boundary due to ease of hydrogen ion penetration from caries process

Enamel Caries (8)

Zone 2 - dark zone 1. does not transmit polarized light 2. caused by presence of lots of tiny pores which are too small to absorb quinoline (polarized light) 3. air / vapor filled pores - opaque 4. pore volume - 2 to 4 % 5. remineralization - increase in size of dark zone 6. size of dark zone - indication of amount of remineralization

Enamel Caries (9)

Zone 3 - body of lesion 1. largest portion of lesion in demineralization phase 2. largest pore volume - 5% at periphery 25% at center 3. straie of Retzius well marked 4. first penetration of caries enters enamel via the striae of Retzius which provides access to rod prism cores 5. BACTERIA may enter if pores large enough

Enamel Caries (10)

Zone 4 - surface zone 1. relatively unaffected by caries attack 2. lower pore volume than body of lesion 3. radiopacity - similar to unaffected enamel 4. surface in contact with saliva hypermineralized by fluoride 5. serves as barrier to bacterial invasion arresting caries process may result in rough, but hard surface

Dentin Caries (1)

This stage of caries progression requires a different mixture of bacterial colonies than is necessary for enamel caries. Bacteria strains capable to produce large amounts of proteolytic & hydrolytic enzymes, rather than acid-producing types of enamel caries.

Ref. 1

Dentin Caries (2)

Dentin caries advance through 3 changes 1. weak organic acid demineralizes dentin 2. organic material of dentin (mostly collagen) is degenerated and dissolved 3. loss of structural integrity followed by bacterial invasion

Dentin Caries (3-1)

Enamel

Dentin

Five microscopic zones

5 4 3 2 1

Ref. 1

Dentin Caries (3-2)

Zone 1: deepest zone, fatty degeneration the earliest changes where bacterial enzymes in dentinal tubules causing breakdown of cell membrane of dentin releasing lipid Zone 2: translucent zone, a band of hypermineralized dentin and sclerotic Zone 3: demineralization, softer dentin due to bacterial enzymes Zone 4: brown discoloration, reduction of mineral with bacteria within dentinal tubules Zone 5: cavitation, no mineralization and organic component is partially dissolved by the bacteria

Bacteria in dentin tubules

Liquefaction
Ref. 1

Dentin Caries (4)

Dentin - 5 zones of slowly progressing lesion Zone 1 - Normal dentin Zone 2 - Subtransparent dentin (affected) Zone 3 - Transparent dentin Zone 4 - Turbid dentin (in advanced lesions - infected) Zone 5 - Infected / Necrotic dentin

Dentin Caries (5)

Zone 1 - Normal dentin  dentinal tubules with smooth odontoblastic  no crystals in lumen  NO BACTERIA in tubules  stimulation - elicits pain

Dentin Caries (6)

Zone 2 - Subtransparent dentin  AFFECTED - not infected  zone of demineralization - by acid from caries  capable of remineralization  damage to odontoblastic processes  NO BACTERIA  stimulation - elicits pain

Dentin Caries (7)

Zone 3 - Transparent dentin  softer than normal dentin  AFFECTED - not infected  zone of demineralization - by acid from caries  capable of remineralization  large crystals  NO BACTERIA  stimulation - elicits pain

Dentin Caries (8)

Zone 4 - Turbid dentin  zone of bacterial invasion  filled with BACTERIA  very little mineral present  collagen irreversibly damaged  will not self-repair / no re-mineralization  must be REMOVED

Dentin Caries (9)

Zone 5 - Infected dentin  NECROTIC dentin in advanced lesions  decomposed dentin  lots of BACTERIA  no recognizable dentin structure  no collagen / no mineral  must be REMOVED

Pulpitis
It is an inflammation of the pulpal tissue that may be acute or chronic, with or without symptoms, and reversible or irreversible.

Ref. 1

Reversible Pulpitis
Decision of reversible or irreversible pulpitis 1. Conservatively restore the defective tooth structure 2. Removed the disease pulp disease 3. Remove the entire tooth

1. Whether pain is spontaneous or stimulated 2. Duration of pain 3. Nature of pain described by patient

Ref. 7

Reversible Pulpitis
Reversible pulpitis / hyperemia limited inflammation of pulp tooth can recover - if caries producing irritant removed ASAP clinically - pain that lingers <10 seconds hyperemia = increased blood flow and volume pulp surrounded by dentinal walls which limits drainage of this increased blood flow/ volume

Irreversible Pulpitis

Inflammation of pulp Tooth can NOT recover if caries producing irritant removed ASAP Clinically - pain that lingers > 10-15 seconds Throbbing, continuous pain Pain upon heat relieved by cold Partial / total pulp necrosis Treatment endo / extraction Ref. 3

Differences between Pain Symptoms Reversible

Elicited Sharp < 20 minutes duration Unaffected by body position Easily localized

Irreversible
Spontaneous Dull > 20 minutes duration Affected by body position Difficult to localize

Refs. 1, 3

Pulp Necrosis
It is the term applied to pulp tissue that is no longer living A result of a sudden trauma (e.g. a blow to the tooth in which blood supply has been severed), there will be no symptoms for a time

Discoloration of tooth

Ref. 1

Common Diagnostic Techniques (1)

1. History and nature of the pain 2. Reaction to thermal changes 3. Reaction to mild electric stimulation 4. Reaction to percussion of the tooth 5. Radiographic examination 6. Visual clinical examination 7. Palpation of the surrounding tissue

Common Diagnostic Techniques (2)

History and Nature of Pain
Reversible pulpitis: sharp and intense Irreversible pulpitis: dull, nagging, vague in location

Common Diagnostic Techniques (3)

Reaction to Thermal Changes
Reversible pulpitis: immediate, sharp pain, last for up to 20 minutes Irreversible pulpitis: less sharp, last for a much longer time

Common Diagnostic Techniques (4)

Reaction to Electric Stimulation
Reversible pulpitis: nerves will be easily excited respond at a lower than normal voltage Irreversible pulpitis: nerves severely damaged a higher level of voltage

Common Diagnostic Techniques (5)

Reaction to Percussion of Tooth
Percussion pain indicates an inflammation in the apical periodontal tissue. It is useful when pain is vague and offending tooth is not apparent.

Common Diagnostic Techniques (6)

Radiographic Examination
It is useful to determine if the inflammatory response has reached the periapical tissue. The presence of a radiolucency at tooth apex is a great help to determine the vague pain in mandible or maxilla.

Common Diagnostic Techniques (6)

Radiographic Examination

Ref. 4

Common Diagnostic Techniques (6)

Radiographic Examination

Ref. 4

Common Diagnostic Techniques (6)

Radiographic Examination

Ref. 3

Common Diagnostic Techniques (6)

Radiographic Examination

Ref. 3

Common Diagnostic Techniques (6)

Radiographic Examination

Ref. 3

Common Diagnostic Techniques (6)

Radiographic Examination

Ref. 3

Common Diagnostic Techniques (7)

Visual Examination
It may reveal a cortical expansion of alveolar bone A small, raised, reddish papule (parulis) over tooth apex indicating an opening of the sinus tract of periapical abscess

Ref. 1

Common Diagnostic Techniques (8)

Palpation of Surrounding Tissues
It indicates that the inflammation has reached the tissue surround tooth apex This is an indication that pulp is necrotic required treatment

Histopathology of Pulpal Disease

Acute Pulpitis

Pulp horn

Intrapulpal hemorrhage
Ref. 1

Histopathology of Pulpal Disease

Chronic Pulpitis
Spherical calcification

Dystrophic (linear) calcification

Ref. 1

Histopathology of Pulpal Disease

Chronic Hyperplastic Pulpitis
1. It is a rare condition that is primarily confined to the molars of children 2. It is the result of rampant acute caries in young teeth that quickly reaches the pulp before it becomes completely necrotic.

Ref. 1

Periapical Lesions
Major factors involve
Presence of an open or closed pulpitis Virulence of the involved microorganisms Extent of sclerosis of the dentinal tubules Competency of the host immune response

Chronic Apical Periodontitis

It is the earliest radiographic evidence of extension of the inflammatory process from the pulpal chamber into the adjacent periodontal membrane around the apical foramen

Chronic

Acute

Chronic apical periodontitis Periapical granuloma Periapical cyst

Periapical abscess Osteomyelitis Chronic Cellulitis Garre Osteomyelitis Osteomyelitis Ref. 1

Periapical Granuloma
1. It occurs when a pulpitis progresses into a periapical lesions 2. The most common lesion occurs after pulpal necrosis 3. It is usually painless, progresses slowly, and seldom becomes very large

Radiography
Well-defined radiolucency with corticated outline

Ref. 1

Periapical Granuloma
Histopathology
Remodeling cortical bone Fibrous tissue Granulation tissue

Root apex

Ref. 1

Periapical Cyst
1. It is a common development of long-standing, untreated periapical graunoma 2. The epithelial lining is derived from rests of Malassez 3. The rests are stimulated to proliferate by low-grade inflammation of the periapical granuloma

Histopathology
Epithelial proliferation

Cystic space

Epithelial distintegration Ref. 1

Periapical Cyst
Histopathology
Cystic lumen
Epithelial lining

Cholesterol Fibrous capsule

Ref. 1

Periapical Cyst
Radiography

Ref. 1

Acute Periapical Conditions

Factors associated
Young tooth with open tubules Rampant caries Closed acute pulpitis Presence of high virulent microorganisms Weakened host defense system

Ref. 3

Periapical Abscess
1. It is the initial lesion that develops when the circumstances are adverse. 2. The most painful patient condition and is potentially one of the most dangerous 3. Progression of acute pulpitis that has exudates extending to adjacent soft and hard tissues.

Histopathology

Ref. 1

Periapical abscess

Ref. 7

Periapical abscess

Ref. 7

SUMMARY (1)

DENTAL CARIES
Epidemiology Clinical Types Enamel Caries Dentin Caries

SUMMARY (2)