Pulpal and Periradicular Lesions (1) PDF

PULPAL AND PERIRADICULAR LESIONS (1) DR. RASHA AHMED ABOU SAMRA  The dental pulp is a unique connective tissue with vascular, lymphatic, and nervous elements that originates from neural crest cells.  The pulp contains odontoblasts, fibroblasts, undifferenti...

PULPAL AND PERIRADICULAR LESIONS (1) DR. RASHA AHMED ABOU SAMRA  The dental pulp is a unique connective tissue with vascular, lymphatic, and nervous elements that originates from neural crest cells.  The pulp contains odontoblasts, fibroblasts, undifferentiated mesenchymal cells and collagen. Dental pulp is an un-mineralized tissue composed of: 1. Soft connective tissue. 2. Vascular components. 3. Lymphatic components. 4. Nerve elements. Dental pulp stem cells (DPSCs) can be found throughout the dental pulp. PULP–DENTIN COMPLEX  Odontoblasts arranged peripherally in direct contact with dentin matrix.  This close relationship between odontoblasts and dentin is known as “pulp–dentin complex” Schematic representation of pulp-dentin complex. The pulp dentin junction shows that peripheral nerve endings of pulp extend into the dentinal tubules. Pulpal Blood Supply The pulp receives its blood supply from end arteries, and the main blood supply goes through the apex such that there is no collateral blood circulation. Diagram showing circulation of pulp INNERVATION OF PULP  Nerve fibers are classified according to their diameter, velocity of conduction, and function.  Fibers having largest diameter are classified as A-fibers while those having smallest diameter are classified as C-fibers.  Aδ fibers are faster conducting and are responsible for localized, sharp dentinal pain.  C-fibers are slower conducting and are responsible for dull and throbbing pain. Features of pulp, which distinguish it from tissue found elsewhere in the body:  Pulp is surrounded by rigid walls and so is unable to expand in response to injury as a part of inflammatory process.  There is minimal collateral blood supply to pulp tissue which reduces its capacity for repair following injury. Features of pulp, which distinguish it from tissue found elsewhere in the body:  Due to presence of the specialized cells (odontoblasts and other cells which can differentiate into hard tissue secreting cells), pulp retains its ability to form dentin throughout life.  Odontoblasts present in the pulp have ability to form dentin in response to caries and irritants. Regenerative capacity of the dentin-pulp complex upon a carious lesion. 1) Reactionary dentin is deposited by surviving odontoblasts in response to a mild insult (e.g. dentin injury by minor caries without pulp tissue exposure). 2) Reparative dentin is secreted by newly formed odontoblast-like cells that originate from dental pulp stem cells in response to severe insult. Schematic diagram of tertiary dentin formation. FUNCTIONS OF PULP Four basic functions of pulp: 1. Formation of dentin. 2. Nutrition of dentin. 3. Innervation of the tooth. 4. Defense of the tooth. Pulpal Response to Inflammation 1. Inflammatory reactions lead to increased vascular permeability. 2. The escaping fluid accumulates in pulp interstitial space. 3. Since space in the pulp is confined, so pressure within pulp chamber rises. 4. In severe inflammation, lymphatics are closed resulting in continued increase in fluid and pulp pressure which may result in pulp necrosis. Pulpal tissue may remain inflamed for long periods and may undergo eventual or rapid necrosis. This change depends on several factors: (1) The virulence of the microorganisms. (2) Host resistance. (3) The amount of circulation and the ability to circulate inflammatory fluids to avoid a marked increase in intrapulpal pressure. (4) Lymphatic drainage. Subsequently, microorganisms or their byproducts and other irritants from the necrotic pulp diffuse from the canal to the periapical region, resulting in the development of an inflammatory lesion.  Etiology of Pulpal and Periapical Diseases (1) Mechanical Irritants 1. The removal of tooth structure without proper cooling may also cause pulp inflammation. 2. Deep scaling and curettage may injure apical vessels and nerves, resulting in pulpal damage. 3. Application of forces beyond the physiologic tolerance of the periodontal ligament (PDL) during orthodontic tooth movement results in disturbance of the blood and nerve supply of the pulp tissue.  Etiology of Pulpal and Periapical Diseases (1) Mechanical Irritants 4. Periapical tissues can be mechanically irritated and inflamed by:  Trauma.  Over-instrumentation of root canals. Inaccurate determination of the working length is usually the cause of over-instrumentation and subsequent inflammation.  Overextension of root canal filling materials. lack of an adequate apical resistance form created during cleaning and shaping can cause overextension of filling materials into the periapical tissues.  Perforation of the root.  Etiology of Pulpal and Periapical Diseases (2) Chemical Irritants Some of the dental materials can cause inflammatory changes in the underlying dental pulp and periapical tissues.  Cavity cleansers, such as alcohol, chloroform, hydrogen peroxide, and various acids.  Cavity liners and bases.  Irrigants used during cleaning and shaping of root canals, intracanal medications, and some compounds present in obturating materials are examples of potential chemical irritants to periapical tissues.  Etiology of Pulpal and Periapical Diseases (3) Microbial Irritants Most common cause of pulpal injury is bacteria or their by-products which may enter the pulp through a break in dentin from:  Caries.  Fracture.  Marginal gap around a restoration.  Or may be due to extension of infection from gingival sulcus. (3) Microbial Irritants The main cause of pulp and periapical disease is the presence of bacteria in the tooth.  Bacteria can enter the dentine-pulp complex via various pathways such as through caries, cracks, fractures, and broken-down restoration margins.  The pulp initially attempts to wall off the The pathways of entry for microorganisms invading bacteria and their endotoxins with into the root canal in cases of pulp necrosis. reparative or reactionary dentine. (3) Microbial Irritants  The formation of reactionary or reparative dentine is the pulp’s attempt to wall itself off from the irritant bacteria and their by-products.  However, the pulp is not able to maintain this function indefinitely.  At some stage, it will fail to resist the bacterial invasion.  It initially becomes inflamed and then Adverse pulpal reactions to caries, subsequently it necroses and becomes infected. trauma or iatrogenic injury. (3) Microbial Irritants Pulpal and periapical pathoses do not develop without the presence of bacterial contamination. The role of bacteria in pulp disease was clearly demonstrated using a ‘germ-free’ rat model. There were no bacteria present in the ‘germ-free’ rats, the pulps were mechanically exposed and left open to the oral cavity.  In the germ-free rats, minimal inflammation only occurred throughout the 72-day observation period. Further, pulpal tissue in these animals was not devitalized.  In contrast, in conventional rats, infection, pulpal necrosis, and abscess formation occurred by the eighth day. (3) Microbial Irritants A. No inflammation is seen in an exposed pulp of a germ-free rat. B. Periapical lesion is apparent in a conventional rat after pulp exposure.  The pulp, root canal, and periapical/periradicular tissues are all inter-related and the conditions within the pulp or root canal have a direct effect on the periapical and periradicular tissues.  When diagnosing endodontic conditions, there are four essential elements that must be determined. 1. The involved tooth. 2. The state of the pulp. 3. The state of the periapical/periradicular tissues. 4. The cause of the disease.  If the condition of any tissue is missing, then the diagnosis is incomplete. Pathways of communication between the pulp and the periradicular tissues.  The main pathway is via the apical foramen.  Other pathways include the dentinal tubules, accessory canals (including lateral and chamber canals and apical delta), developmental defects, cracks, and fractures of the tooth.  Hence, the state of the pulp directly affects the periradicular tissues. “Peri-radicular” versus “Periapical”? It is more appropriate to use the term “peri-radicular” In the literature, the general heading of “periapical disease” is often used. However, the periapical region is only one small part of the tissues that surround the entire tooth root, all of which can respond or react to pulp inflammation and infection of the root canal system–that is, such responses are not restricted to the periapical region. Periradicular conditions are a direct result of pulp and root canal diseases  Whenever there is inflammation or infection within the root canal system, the periapical tissues become inflamed.  The inflammation can then progress and other conditions can develop, such as infections and cysts.  Hence, periradicular conditions are indirectly caused by bacteria from the oral cavity that enter the pulp and root canal system through caries, cracks, fractures, and breakdown of restoration margins. The Development and Progression of Pulp and Root Canal Conditions Whenever any tissue in the body is injured or irritated The first reaction will be inflammation. If there is no treatment provided to remove the irritating factor, the tissue will necrose. Then it will become infected. The stages of disease progression when any Over time, there will be loss of the necrotic tissue of the body is irritated or injured and tissue as the bacteria digest and remove it. no treatment is provided The Development and Progression of Pulp and Root Canal Conditions Irritation of the pulp The pulp’s first response to irritation is forming various forms of dentine If the bacteria are not removed (i.e. no dental treatment is done), the pulp will become inflamed (i.e. pulpitis) Over time (if still untreated), the pulp will be necrotic The stages of disease progression within the pulp and root canal system when a tooth is subject to bacterial invasion and no treatment is provided  The first stage of pulp disease is inflammation, which is known as pulpitis.  Reversible pulpitis is considered to be a milder form of inflammation, with relatively mild symptoms, and conservative treatment will resolve the inflammation.  If a tooth with reversible pulpitis is not treated, then the inflammation will continue to develop and spread throughout the pulp to become irreversible pulpitis.  Some patients with irreversible pulpitis may not seek treatment as the pain may not be severe, or the pain may subside in a short period of time. This occurs when the pulp starts to necrose. The processes of pulp necrosis and infection occur simultaneously in teeth with the ‘bacterial front’ moving through the pulp, from the pulp chamber through the root canal, and towards the apical foramen.  Apical to the ‘bacterial front,’ the pulp tissue will be irreversibly inflamed.  Coronal to this ‘front,’ the tissue will be necrotic and infected. Once the entire pulp is necrotic and infected, and within a relatively short period of time, the necrotic tissue will be removed by the bacteria and the root canal system becomes pulpless and infected. When the term ‘chronic’ is used as part of a clinical diagnosis  It implies that there are no symptoms or only mild symptoms present.  The problem has been present for a long time (Weeks, months, or even years) and the patient may only mention it ‘in passing’ when they attend for a routine dental examination. In contrast, when the term ‘acute’ is used as part of a clinical diagnosis  It implies that there is some urgency about the matter.  The patient typically has moderate or severe pain and this pain may only have been present for a short time (Several hours or a few days). These clinically defined terms are commonly used in medicine and dentistry. They should not be confused with the same terms when used as descriptors for the histological assessment of inflamed tissues Other terms that have become popular in recent years are ‘symptomatic’ and ‘asymptomatic’ to replace ‘acute’ and ‘chronic,’ respectively, even though these terms are not used elsewhere in the dental or medical literature Schematic representation of the progression of pulp and root canal conditions through the various stages of the disease process Classification of the Conditions of the Pulp and Root Canal System  PULP AND ROOT CANAL CONDITIONS (1) Clinically Normal Pulp The term “clinically normal pulp” is used for a pulp that has no signs or symptoms to suggest that any form of disease is occurring and the tooth does not have any pulp pathosis that requires treatment.  Typical symptom: no symptoms.  Clinical findings:  Normal reaction to cold and electric pulp sensibility tests.  Sensation is felt but disappears immediately upon removal of the thermal stimulus.  Percussion and palpation are normal.  Radiographic findings: no evidence of resorption, caries, no radiographic signs of pathosis; normal periodontal ligament (PDL) space and lamina dura.  Associated periradicular conditions: clinically normal periapical tissues.  PULP AND ROOT CANAL CONDITIONS (2) PULPITIS This is a clinical and histologic term denoting inflammation of the dental pulp. CLINICALLY DESCRIBED AS: A. Reversible pulpitis. B. Irreversible pulpitis. HISTOLOGICALLY DESCRIBED AS:  Acute.  Chronic.  Hyperplastic. (A) REVERSIBLE PULPITIS Definition: Reversible pulpitis is mild inflammatory condition of pulp caused by noxious stimuli in which the pulp is capable of returning to normal state following removal of stimuli. Etiology 1. Caries. 2. Exposed dentin. 3. Recent dental treatment. 4. Defective restorations with marginal leakage. 5. Thermal injury: Tooth preparation with dull bur without coolant Overheating during polishing of a restoration Preparing teeth for restorations may generates frictional heat. Such injury Keeping bur in contact with teeth too long is lessened by proper water irrigation during the cutting procedure. (A) REVERSIBLE PULPITIS Symptoms:  Clinically, the patient with reversible pulpitis usually has mild symptoms expressed as increased sharp pain with thermal changes (commonly caused by cold stimuli).  The pain is short in duration.  Following insertion of a deep restoration, patient may complain mild sensitivity to temperature changes, especially cold. Such Insertion of deep restoration may cause sensitivity may last for a week or longer but gradually, it pulp inflammation. subsides. This sensitivity is symptom of reversible pulpitis. (A) REVERSIBLE PULPITIS  Radiographic examination: Shows normal PDL and lamina dura.  Diagnosis: Thermal pulp sensibility tests can reproduce the pain associated with heat and/or cold stimuli; pain with thermal testing will be sharp, and of short duration after removal of the stimulus.  Treatment:  Correction of the clinical problem that caused reversible pulpitis results in healing and resolution of symptoms.  Conservative removal of caries, protection of dentin, and a proper restoration will typically resolve the symptoms. (A) REVERSIBLE PULPITIS Conservative treatment will resolve the inflammation. Removing the cause of the pulp irritation – such as caries, a crack, or a restoration that is breaking down – and then either restoring the tooth again or placing a sedative lining and an interim restoration to allow time for pulp healing, plus time to reassess the pulp status. Pulp sensibility tests would indicate if the pulp has returned to a clinically normal state. Dentin hypersensitivity Confusion can occur when there is exposed dentin, without evidence of pulp pathosis, which can sometimes respond with sharp, quickly reversible pain when subjected to thermal, evaporative, tactile, Dentinal tubules are filled with mechanical, osmotic, or chemical stimuli. This is fluid that, when stimulated, will cause sensation. Temperature known as dentin hypersensitivity. Exposed dentin in changes, air, and osmotic changes can provoke the odontoblastic the cervical area of the tooth accounts for most of process to induce the stimulation of underlying A-delta fibers. the cases diagnosed as dentin sensitivity.  DENTIN HYPERSENSITIVITY AND ITS MANAGEMENT The dentin is hypersensitive most likely due to: 1. Lack of protection by cementum. 2. Hydrodynamic movement of fluid in dentinal tubules. Patent dentinal tubules are present in areas of hypersensitivity and may result in localized reversible inflammation of the pulp at the sites involved.  MANAGEMENT OF DENTIN HYPERSENSITIVITY 1. The application of tubule blocking agents usually alleviates the condition, at least temporarily. 2. Contemporary desensitizing agents that have been found to be effective include:  Nanohydroxyapatite.  Laser treatment. (B) IRREVERSIBLE PULPITIS As the disease state of the pulp progresses, the inflammatory condition of the pulp can change to irreversible pulpitis. At this stage, treatment to remove the diseased pulp will be necessary. This condition can be divided into the subcategories of symptomatic and asymptomatic irreversible pulpitis. IRREVERSIBLE PULPITIS 1. ASYMPTOMATIC 2. SYMPTOMATIC IRREVERSIBLE IRREVERSIBLE PULPITIS PULPITIS 1. ASYMPTOMATIC IRREVERSIBLE PULPITIS This is a clinical diagnosis based on subjective and objective findings indicating that the vital inflamed pulp is incapable of healing and that root canal treatment is indicated. However, the patient does not complain of any symptoms. In asymptomatic irreversible pulpitis the tooth has:  Deep caries or tooth structure loss.  Deep caries will not produce any symptoms, even though clinically or radiographically the caries may extend well into the pulp.. These cases may have deep caries that would likely result in exposure following removal. 1. ASYMPTOMATIC IRREVERSIBLE PULPITIS Treatment of asymptomatic irreversible pulpitis Root canal treatment should be performed as soon as possible so that symptomatic irreversible pulpitis or necrosis does not develop and cause the patient severe pain and distress.  The tooth may become IF ASYMPTOMATIC symptomatic IRREVERSIBLE PULPITIS LEFT UNTREATED The pulp will become necrotic 2. SYMPTOMATIC IRREVERSIBLE PULPITIS “It is a persistent inflammatory condition of the pulp, caused by a noxious stimulus.” This is a clinical diagnosis based on subjective and objective findings indicating that the vital inflamed pulp is incapable of healing 2. SYMPTOMATIC IRREVERSIBLE PULPITIS Etiology Irreversible pulpal inflammation can result from: 1. Dental caries (most common cause). 2. Chemical, thermal, mechanical injuries of pulp. 3. Untreated reversible pulpitis. Secondary caries beneath restoration causing pulpal exposure. Deep dental caries causing exposure of pulp. 2. SYMPTOMATIC IRREVERSIBLE PULPITIS Symptoms: 1. Deep restorations, caries, pulp exposure may be present. 2. Intermittent or spontaneous pain. 3. Teeth are sensitive to thermal triggers. Exposure to extreme temperatures, especially cold, will elicit intense and prolonged episodes of pain, pain lingers even after the thermal stimulus has been removed. 4. The pain may be sharp or dull, localized, diffuse, or referred to other sites. 5. Pain exacerbated on lying down due to elevation of pulpal blood pressure.Pain may be so severe that it keeps the patient awake at night.  2. SYMPTOMATIC IRREVERSIBLE PULPITIS Thermal test: The pulp responds more readily to cold stimulation than for normal tooth, with prolonged episodes of pain even after the thermal stimulus has been removed. (lingering pain even after removal of the stimulus ) Radiographically: 1. Typically, there are minimal or no changes in the radiographic appearance of the periradicular bone. 2. With advanced irreversible pulpitis, a thickening of the periodontal ligament may become apparent on the radiograph. 2. SYMPTOMATIC IRREVERSIBLE PULPITIS Treatment: Root canal treatment. When symptomatic irreversible pulpitis remains untreated, the pulp will eventually become necrotic. Mandibular left first molar had deep mesio-occlusal caries. Patient complained of sensitivity to hot and cold liquids initially but later pain became spontaneous. EPT test showed lingering pain even after removal of the stimuli. Response to both percussion and palpation was normal. Diagnosis: symptomatic irreversible pulpitis. Treatment given was nonsurgical endodontic treatment followed by a permanent restoration.  2. SYMPTOMATIC IRREVERSIBLE PULPITIS Intrapulpal injection  In some cases of symptomatic irreversible pulpitis intrapulpal injection may be needed.  The pulp must be exposed to allow direct intrapulpal injection.  The needle should be firmly wedged into the chamber or canal 2. SYMPTOMATIC IRREVERSIBLE PULPITIS Advantages of the intrapulpal injection: 1. It produces profound anesthesia if it is given under pressure. 2. The onset of anesthesia is immediate. 3. No special syringes or needles are required. Disadvantages of the intrapulpal injection: 1. The major drawback of the intrapulpal injection technique is that the needle and injection are made directly into vital and very responsive pulp tissue; this injection is moderately to severely painful. 2. Another disadvantage of the technique is the duration of pulpal anesthesia (15 to 20 minutes). The pulpal tissue must be removed quickly and completely to prevent a recurrence of pain during instrumentation.  2. SYMPTOMATIC IRREVERSIBLE PULPITIS  For emergency management of vital teeth that are not initially sensitive to percussion, occlusal reduction has not been shown to be beneficial.  In vital teeth in which the inflammation has extended periapically, which will present with pretreatment pain to percussion, occlusal reduction has been reported to reduce post-treatment pain. (C) Chronic Hyperplastic Pulpitis  It is an inflammatory response of pulpal connective tissue due to extensive carious exposure of a young pulp.  It shows overgrowth of granulomatous tissue into carious cavity. Etiology Hyperplastic form of chronic pulpitis is commonly seen in teeth of children and adolescents because in these pulp tissue has high resistance and large carious lesion permits free proliferation of hyperplastic tissue.  Chronic Hyperplastic Pulpitis ( a ) Cut surface showing soft tissue mass protruding from pulp cavity. ( b ) Histology shows granulation tissue covered with squamous epithelium (C) Chronic Hyperplastic Pulpitis Signs and Symptoms  It is usually asymptomatic.  Fleshy pulpal tissue fills the pulp chamber.  It is less sensitive than normal pulp but bleeds easily due to rich network of blood vessels.  Sometimes this pulpal growth interferes with chewing. (C) Chronic Hyperplastic Pulpitis Diagnosis  Hyperplastic form shows a fleshy, reddish pulpal mass which fills most of pulp chamber or cavity.  It is less sensitive than normal pulp but bleeds easily when probed.  Tooth may respond or not to thermal test, unless one uses extreme cold. More than normal current is required to elicit the response by electric pulp tester. (C) Chronic Hyperplastic Pulpitis Treatment  In case of hyperplastic pulpitis, removal of polypoid tissue using periodontal curette or spoon excavator followed by root canal treatment.  If tooth is at non-restorable stage, it should be extracted. Pulp Necrobiosis  A tooth with necrobiosis has both inflamed (acute irreversible pulpitis) and necrotic (usually infected) pulp tissue.  Many dentists use “partial necrosis” for this stage of the disease process.  Grossman suggested the term “necrobiosis” because it more accurately indicates the condition.  “necro” indicating necrosis.  “bio” indicating live tissue. Pulp Necrobiosis  The necrotic tissue may be in the pulp chamber with the inflamed tissue in the root canal, or the different conditions may exist in different canals of a multi- rooted tooth.  Teeth with this condition are difficult to diagnose since they often present with a mixture of the symptoms and signs of both pulpitis and necrosis with infection.  Typically, this stage of the disease process is only present for a short time— perhaps a few hours only or up to a few days.  As the bacterial front moves apically so the entire pulp becomes necrotic.  (3) PULP NECROSIS  This is a clinical diagnostic category indicating death of the dental pulp.  Pulp necrosis or death is a condition subsequent to untreated symptomatic or asymptomatic irreversible pulpitis and usually occurs over a variable period of time.  On rare occasions such as trauma, the onset of necrosis may be sudden and immediate.  The pulp is usually nonresponsive to pulp testing.  When pulpal necrosis occurs, the pulpal blood supply is nonexistent and the pulpal nerves are nonfunctional. (3) PULP NECROSIS  With pulp necrosis, usually the tooth will not respond to electric pulp tests or to cold stimulation.  However, if heat is applied for an extended period of time, the tooth may respond to this stimulus. This response could possibly be related to remnants of fluid or gases in the pulp canal space expanding and extending into the periapical tissues.  After the pulp becomes completely necrotic, the tooth will typically become asymptomatic until such time when there is an extension of the disease process into the periradicular tissues.  (3) PULP NECROSIS  Pulpal necrosis may be partial or complete and it may not involve all of the canals in a multirooted tooth. For this reason, the tooth may present with confusing symptoms. Pulp testing over one root may give no response, whereas over another root it may give a positive response. The tooth may also exhibit symptoms of symptomatic irreversible pulpitis.  After the pulp becomes necrotic, microbial growth can be sustained within the canal. When this infection extends into the periodontal ligament space, the tooth may become symptomatic to percussion or exhibit spontaneous pain. (4) Internal Resorption Internal resorption is an idiopathic resorption occurring in dentin of the pulp chamber or root canals of the teeth. Etiology Exact etiology is unknown (Idiopathic). Patient may present history of trauma or persistent Schematic representation of ballooning of pulpal cavity showing pulpitis. internal resorption of the tooth (4) Internal Resorption (4) Internal Resorption Symptoms  Usually asymptomatic, recognized clinically through routine radiograph.  Pain occurs if resorption perforates the root.  Pink tooth” is the pathognomonic feature of internal root resorption in the pulp chamber.  In actively progressive lesion, pulp is partially vital and may show Internal resorption symptoms of pulpitis. of tooth causing perforation of root.  Pulp shows either partial or complete necrosis. (4) Internal Resorption For internal root resorption to continue, the pulp tissue apical to the resorptive lesion must have a viable blood supply; this provides clastic cells and their nutrients, and the infected necrotic coronal pulp tissue provides stimulation for those clastic cells. Therefore, the pulp apical to the site of resorption must be vital for the resorptive lesion to progress. (4) Internal Resorption Diagnosis Clinically: “Pink spot” appearance if the resorption is in the dentin of the pulp chamber. Pulp tests: Positive, if coronal portion of pulp is necrotic, apical pulp could be vital. Radiographic changes:  Classical description of internal resorption, that is, clearly well-defined radiolucency of uniform density which balloons out of root canal.  Bone changes are seen only when root perforation into periodontal ligament takes place (4) Internal Resorption Treatment  Pulp extirpation stops internal root resorption  Surgical treatment is indicated if conventional treatment fails. If left untreated, the pulp tissue apical to the resorptive lesion undergoes necrosis and the bacteria infect the entire root canal system, resulting in apical periodontitis.