Pulpal Diseases08india

PULPAL DISEASES and PERIAPICAL DISEASES Peng Bin

Conception Definitions Pulpal diseases Periapical diseases Relationships Anatomy—foramen Etiology—caries Pathology—inflammation Symptom—pain Treatment—root canal therapy

Endodontic Therapy —Weine Clinical Endodontics —Tronstad Pathways of the Pulp —Cohen Endodontics —Ingle



Histophysiology of the dental pulp



Etiology



Pulpal diseases



Periapical diseases

Histophysiology of the dental pulp Special environment The dental pulp is one kind of loose connective tissues, and the respond to changes in environment should be the same as any other loose connective tissue. However, the dental pulp has an unique environment.

1 、 A low-compliance environment 2Painful 、 Resilience of the connective tissue (resilient fiberIrreversible reinforced ground substance ) 3 、 Ineffective collateral circulation

Four zones  The

dentinoblastic zone

 The

cell-free zone (cell-poor zone,

zone of Weil, subdentinoblastic zone)  The

cell-rich zone

 The

central zone (pulp proper)

Structural elements The components of dental pulp consist of cells, intercellular substance and intercellular fluid. fibroblasts, reserve cells, defense cells, special cells.

Cells The fibroblast, the principal cell distributed throughout the pulp, is specially abundant in the cell-rich zone. It produces gelatinous intercellular matrix and collagen fibers (Type Ⅲ collagen, partly Type Ⅰ). young fibroblasts—mitosis—dentinoblasts

With increasing age, there is a diminution in the size and number of these cells, and caries, abrasion, or pulp capping can accelerate this process.

The reserve cell, found principally along capillaries and in the cell-rich zone, is a primitive undifferentiated cell. fibroblasts dentinoblasts macrophages dentinoclasts

The defense cell, including macrophages, dendritic cells, lymphocytes and mast cells, is in the normal pulp. 

engulf bacteria, foreign body, and dead cells



participate in immune reactions

The dentinoblast(odontoblast), a highly specialized connective tissue cell of the dental pulp, plays an unique role in both dentin and pulp function. dentinoblast odontoblast

The dentinoblasts form a palisade arrangement at the pulp periphery. The side and shape of the cells varies on their location: high columnar – pulp chamber low columnar & cuboidal – cervical or midroot area flattened – apex

The dentinoblasts do not undergo mitosis and may therefore be considered postmitotic, or end cells. When they die, their function is carried out by neighboring dentinoblasts or by new dentinoblasts. Since dentin collagen is principally TypeⅠ, it has been suggested TypeⅠ is produced by the dentinoblasts alone.

Intercellular components  Collagen

fibers Type Ⅰ, Ⅲ  Amorphous ground substance matrix mucopolysaccharides(resilient)  Intercellular tissue fluid Inflammation—increased pressure

Functions Formative Nutritive Nervous Defense

functions functions functions functions

Formative function  Primary

dentin (initial)

 Secondary

dentin (functional)

 Reparative

dentin (irregular, defensive,

irritation, tertiary)

Nutritive function The dental pulp must maintain the vitality of the dentin by providing oxygen and nutrients to the dentinoblasts and their processes, as well as providing a continuing source of dentinal fluid.

Defense function  Dentinal  Smear

pain

layer

 Tubular

sclerosis

 Reparative

dentin formation

 Inflammation

Nervous function Vasomotor control—motor nerves Defense pain—sensory nerves

Table 1

Pain fibers in the pulp A-δ fibers

Diameter(μm) 2-5 Conduction velocity(m/s) 5-30 Myelinated yes/no Location of terminals superficial Pain characteristics

sharp, pricking, unpleasant, bearable Stimulation threshold relatively low

C-fibers 0.3-1.2 0.4-2 no near vessels throughout pulp throbbing, aching, less bearable high threshold

Table 2 Stimulus

Responses of the Pain fibers to special stimuli A-δ

Intrapulpal pressure changes sudden nerve compression increased proloned nerve compression decreased Vitality tests electric positive# cold positive rapid heat first# slow and sustained heat negative Resistance to oxygen depletion short survival

C increased continued negative# negative second# positive longer survival

Etiology  Microbial

agents  Physical agents  Chemical agents  Others

Microbial agents Role

of bacteria Pathways of the infections Responses of the tissues

Role of bacteria History In 1890, Miller demonstrated the presence of bacteria in necrotic human pulp tissue. In 1965, Kakehashi did a very important experiment. conventional rats -- germ-free rats In 1974, Korzen studied the mixed infection. conventional rats -- gnotobiotic rats

Until the early 1970’, the predominant bacteria are facultative. In the 1980’, root canal infections are multibacterial and that anaerobic organisms, namely Bacteroides species, play a significant role. 10 year’s ago, almost all the infections are mixed and acute symptoms are usually relate to Porphyromonas (Bacteroides) gingivalis, Porphyromonas endodontalis, and Prevotella (Bacteroides) buccae.

Associations with clinical features Pain— Peptostreptococcus species/Prevotella species Swelling— Peptostreptococcus micros/ Prevotella species “Wet” canal— Prevotella species/Eubacteriun species

Pathways Dentinal tubules

There are some important variables that affect the pulpal diffusion of microbial products through dentin:  The

thickness of remaining dentin  The surface area of the exposed dentin  The presence or absence of a smear layer  The potency of the microbial products  The rate of pulpal blood flow

Pulp exposure  Tooth

decay

 Traumatic

injuries  Abrasion  Erosion  Anomalies

Peri

Pulp

DC

Enamel hypoplasia

Periodontal pocket

 Lateral

canals

 Apical

foramina

 Dentin

Anachoresis Definition—a positive attraction of bloodborne microorganisms to inflamed or necrotic tissue during a bacteremia. In 1939, found for the first time anachoretic effect of periapical inflammation in dogs. In 1941, confirmed the similar effect of pulp tissue in rats.

Responses of the tissues Bacteria, their by-products and toxins will cause the responses and damages. Pulpal disease state(formula)= number of bacteria × virulence tissue resistance Inflammation and immune responses

Physical agents Cutting procedures It can produce varying magnitudes of pulpal damage, depending on applied pressure, speed, bur size, temperature, cavity depth, and postoperative insulation protection.

To reduce the damage the operator can control  The

temperature with adequate coolants

 Force

by using smaller cutting tools

 Remaining

dentin thickness with proper cavity depth

 Postoperative

protection with zinc oxideeugenol(ZOE)

Thermal irritants  Cutting  Metal

procedures

fillings without proper insulation

of liners and bases  Polishing

restoration

Other physical irritants  Acute

trauma

 Chronic

trauma (Traumatic occlusion, attrition, bruxism, erosion, abrasion)

 High

fillings, tooth drift, too rapid orthodontic movement

 Improper

using instruments within the root canal or overextension will force dentinal debris, irrigating solutions, and toxic components of necrotic tissue into periapex.

Chemical agents  Disinfecting

chemical (phenol, alcohol, chloroform, hydrogen peroxide, silver nitrate)

 Dentin-conditioning

and dentin-bonding agents(37% phosphoric acid)

 Acid-liquid

components of cements(zinc phosphate cements, silicate cements, glass ionomer cements)

 Eugenol

released from ZOE

 Composite

resins

 Restorative

materials and microleakage

 Using

strong or excessive amounts of interappointment intracanal chemicals may induce periapical inflammation.

Others  Cancer  AIDS,

diabetes

 Internal

or external resorption

 Immunologic

factors

allergies or hypersensitivities

Internal resorption

External resorption

Pulpal diseases Conception Classification Diagnosis

Classification

1. Inflammatory diseases of the dental pulp a. Hyperalgesia(reversible pulpitis, hyperreactive pulpalgia, --) (1) Hypersensitive dentin (2) Hyperemia b. painful pulpitis (1) Acute pulpalgia( acute pulpitis) (2) Chronic pulpalgia(subacute pulpitis) c. Nonpainful pulpitis (1) Chronic ulcerative pulpitis(due to caries) (2) Chronic pulpitis(carious lesion absent) (3) Chronic hyperplastic pulpitis(pulp polyp)

2. Additional pulp changes a. Necrosis( inflammatory or retrogressive changes) b. Retrogressive changes (1) Atrophy and fibrosis (2) Dystrophic calcification c. Internal resorption( chronic inflammation?)

Cohen’s

A normal pulp Reversible pulpitis Irreversible pulpitis Asymptomatic irreversible pulpitis Hyperplastic pulpitis Internal resorption Canal calcification Symptomatic irreversible pulpitis Necrosis ----Pathways of the pulp

Table 3 Classifications of pulpal diseases Loyola Hyperalgesia

Ingle’s

Cohen’s

Hyperreactive pulpalgia

Reversible pulpitis Irreversible pulpitis Symptomatic irreversible Asymptomatic irreversible

Acute pulpitis Acute pulpalgia Chronic pulpalgia Chronic pulpalgia Chronic pulpitis Chronic hyperplastic Hyperplastic pulpitis Hyperplastic pulpitis Pulp necrosis Pulp necrosis Internal resorption Atrophy Atrophic pulposis Canal calcification Dystrophic calcification Calcific pulposis Necrosis

Normal pulp A normal pulp is asymtomatic and produces a mild to moderate transient response to thermal and electrical stimuli. The response subsides almost immediately when the stimulus is removed. The tooth and its attachment apparatus do not cause a painful response when percussed or palpated. Radiographs reveal no calcification or rooth resorption, and the lamina dura is intact.

Reversible pulpitis Definition Reversible pulpitis is an initial and potentially reversible pulpal inflammation. (Hyperalgesia, Hyperreactive pulpalgia, Hypersensitivity) Hypersensitive dentin Hyperemia

Histopathology and symptoms Pulpal hyperemia is a capillary engorgement with a predisposition to edema, and it will increase the intrapulpal pressure in the involved area. The threshold of A-δ nerve fibers is lowered so that the dentin is in a hypersensitive state to external stimuli.

Some mediators (5-hydroxytryptamine, 5HT) initiate pain either direct excitation of the nerve terminals or by lowering their threshold to such stimuli as heat, cold, or mechanical forces.

Diagnosis Pain  Does

not occur spontaneously –asymptomatic

 Requiring

an external stimulus to evoke a

painful response  Sharp

and brief duration, ceasing when the

irritant is removed

Visual examination and history caries, restorations, fractures or traumatic occlusion Radiography the depth of the caries or cavity preparation Percussion negative response Vitality tests thermal testing - cold stimulation, hot electric testing - positive

Acute pulpitis Definition It is a severely painful and irreversible acute inflammatory response characterized by exudative hyperactivity. Painful pulpitis

Acute pulpitis Subacute pulpitis (Chronic pulpalgia)

Histopathology and symptoms If the inflammation(fluid exudation, leukocyte infiltration) continues, the intrapulpal pressure will increase beyond the threshold limit of Cfibers–spontaneous pain. The pain will be maintained and increased by an internal irritant(necrotic tissue)if an external irritant is removed—continuous pain.

Diagnosis Pain  Occurs

spontaneously, and will vary from a mild and readily tolerated discomfort to a severe, even excruciating, throbbing.

It is continuous or has periods of cessation (intermittent). early to late

 lingers

after the primary irritant has been

removed.  Is

generally diffuse and not readily localized by the patient.

 Lying

down or bending over may intensify the pain.

Pain referral Painful pulpitis may be referred to other areas of the same and opposing arches as well as to structures remote from the involved tooth (mandibular premolars to maxillary molars, mandibular molars or the midramal area).

One summary  Pain

is referred to the opposite arch on the same side by posterior teeth only.

 Referral

from incisor to posterior teeth seldom occurs.

 Refrral

found.

of pain across the midline is not

Visual examination and history the involved tooth or a traumatic experience Radiography and Percussion the caries and negative response

Vitality tests(thermal test) the pain will persist after stimulus is removed. cold will tent to relieve the pain in advanced stages of pulpitis when coronal necrosis exists(contractile effect—reduce intrepulpal pressure).

Chronic pulpitis Definition It is not a severely painful, and has a chronic inflammatory response characterized by proliferative activity. nonpainful pulpitis—chronic pulpitis

Histopathology and symptoms Ulcerative form (Ulcerative pulpitis) The pulp is cariously exposed with an abscess formation at the exposed point. Pain is absent because adequate drainage and absorption of the exudate forms.

A. B.

C. D.

The zone of necrosis at exposed pulpal surface The exudative zone with dense PMN and lymhpocytic infiltration. The granulomatous zone of irritant. Noninflamed pulp tissue.

Hyperplastic form (Hyperplastic pulpitis) This chronic inflammation of the cariously exposed pulp is characterized by an overgrowth of granulomatous tissue into the carious cavity. Found in teeth of children and adolescents, and large carious exposure.

A.

Granulomatous tissue(polyp)

B.

Implanted epithelial cells

C.

Pulp chamber wall

Closed form(closed pulpitis) This may occur from operative procedures, trauma, or periodontal lesions,not carious. Depending on the strength and duration of the inciting irritant, pulpitis may be chronic from the onset or become chronic after the acute responses have subsided.

Diagnosis Pain may be absent or little Visual examination and history carious or pulp polyp Radiography and Percussion the caries and negative response Vitality tests normal responses or greater stimulation may be required.

Necrosis Definition Necrosis is the death of pulp tissue, which is a result of acute and chronic inflammation of the pulp or an immediate arrest of circulation by traumatic injury.

Diagnosis Pain absent in a tooth with total necrosis Visual examination and history the involved tooth or a traumatic experience, or definite color change Radiography and Percussion the caries and negative response Vitality tests no responses

Periapical diseases Conception Classification Diagnosis

Classification 1.

Painful pulpoperiapical pathoses a. incipient acute apical periodontitis b. advanced acute apical periodontitis (1) acute periapical abscess (2) recrudescent abscess (3) subacute periapical abscess 2. Nonpainful pulpoperiapical pathoses a. condensing osteitis b. incipient chronic apical periodontitis c. advanced chronic apical periodontitis (1) periapical granuloma (2) chronic periapical abscess (3) periapical cyst

Cohen’s

Acute apical periodontitis Acute apical abscess Chronic apical periodontitis Phoenix abscess Apical cyst Periapical osteosclerosis ----Pathways of the pulp

Painful pulpoperiapical pathoses Definition Acute apical periodontitis—the initial exudative and mildly symptomatic inflammatory reaction of the periapical tissues. Acute periapical abscess—an advanced exudative and severely symptomatic inflammatory response of the periapex.

Histopathology and symptoms The painful symptoms are caused by a great increase in intraperiapical pressure and mediators released by the injured cells. The initial stage—mild pain

The abscess stage—increased pain The most intense pain—the pus penetrates the outer plate of bone and begins to raise the periosteum.(Swelling) The pain will subside once pus inters the space of mucosa.

Diagnosis

Pain  Range

from slight tenderness of the earlier stage to throbbing of the later stage.

 Is

readily localized by the patient.

 Will  The

be increased when percussion.

patient usually can tolerate the discomfort if the tooth is not touched.

Swelling and palpation not present in the early stage, increase as pus extends towards the surface incisors—the lip maxillary canines—the ala of the nose maxillary premolars—the eyelid

Vitality tests usually negative or positive Radiography slight widening of the apical periodontal ligament space or radiolucency

Nonpainful pulpoperiapical pathoses Advanced chronic apical periodontitis

Characteristics Periapical granuloma—the growth of granulation tissue and the presence of chronic inflammatory cells in respose to continued pulpal irritation.

Chronic periapical abscess—longstanding low-grade inflammatory reaction, and formation of a parulis and active pus formation draining by a sinus tract.

Periapical cyst—a central fluid-filled epithelium-lined cavity surrounded by GT and fibrous encapsulation.

Diagnosis (chronic apical periodontitis) Pain ??? percussion Color or sinus tract change to dark, tract opening

Swelling and palpation A slight swelling around the sinus tract stoma—chronic periapical abscess A hard tissue bulge may appear—periapical cyst Vitality tests usually negative

Radiography  give

confirmation of the involved tooth or root

 Classification

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