BDS 10003 pulpal diseases.pdf

BDS10003 Pulpal Diseases Aim: The aim of this lecture is to review the histopathological features of common pulpal disease Objectives: On completion of this lecture, the student should be able to: Understand the histopathological features of acute and chronic pulpal disease Understand the key c...

BDS10003 Pulpal Diseases Aim: The aim of this lecture is to review the histopathological features of common pulpal disease Objectives: On completion of this lecture, the student should be able to: Understand the histopathological features of acute and chronic pulpal disease Understand the key cellular infiltrates of acute and chronic inflammation Normal Pulp The dental pulp is a delicate connective tissue occupying the center of a tooth. It is formed of  collagen fibers,  cells,  nerves,  blood vessels,  lymphatics The inflammatory process in the pulp is basically the same as elsewhere in the body connective tissue Inflammatory process inflammation is a localized physical condition in which part of the body becomes reddened, swollen, hot, and often painful, especially as a reaction to injury or infection 1 2 3 Significance of pulp anatomy in inflammation: The pulp is totally enclosed within hard tissue. →This prevents the normal swelling of tissue that occurs during inflammation (limiting the area for tissue expansion) Thus leading to stagnation or strangulation of the pulp circulation → causing irreparable damage 1. Significance of pulp anatomy in inflammation: 2. Lack of collateral circulation: The blood vessels of the pulp are terminal in type (which weakens the defensive mechanism of the pulp) 3. Nerves, arteries and veins enter through a small apical foramen. On vasodilatation, if the pressure becomes so great that the veins become constricted, the venous blood is prevented, congestion, degeneration and necrosis of the pulp may ensue. Significance of pulp anatomy in inflammation: 4. The pulp lacks the power of regeneration. 5. The nerve supply of the pulp (free nerve endings only) doesn’t permit localization of the offending tooth in cases of pulpitis 6. Response to sudden temperature changes: The range of temperature response extends from 20°C to 45°C [So too hot or too cold stimuli may produce inflammatory pulpal changes. As long as enamel and dentin remain intact they afford sufficient protection to the pulp [physical barrier--efficient insulator] Living irritants Main irritants (microbial) Mechanical irritation Electrical irritation of the pulp Thermal irritation Non living irritants Chemical irritation Classification of pulp inflammation According to severity & duration Focal reversible pulpitis Acute Chronic According to extent of pulp involvement Total Partial According to communication to oral cavity Closed Open Reversible pulpitis level of pulp inflammation in which tissue is capable to return to normal state if the irritant is removed Irreversible pulpitis a higher level of inflammation in which dental pulp has been damaged beyond the point of recovery Focal Reversible Pulpitis: It is a mild inflammatory pulp reaction and is the earliest form of pulpitis [often referred to pulp hyperemia] F.R.P. is regarded as a reversible condition provided the irritant is removed before the pulp is severely damaged. Removal of the cause before The pulp is severely damaged Focal Reversible Pulpitis: Clinical Features:  exhibit mild to moderate pain to thermal changes, particularly cold.  The Pain does not occur without stimulation, it subsides within seconds after removal of the irritant.  Teeth usually show deep carious lesions, large metallic restorations without adequate isolation, or restorations with defective margins.  Teeth are not sensitive to percussion Focal Reversible Pulpitis: Histologic Features: dilation and engorgement of blood vessels (hyperemia). Inflammatory fluid exudates may be seen as vesicles between the cells. Intact odontoblastic layer. Reparative dentin. Intact odontoblastic layer Dilated blood vessels Focal Reversible Pulpitis vasodilated blood vessels Intact odontoblastic layer What will happen if the cause is not eliminated in the proper time? Dilatation of the pulp vessels. Inflammatory fluid exudate escape haemoconcentration and increased viscosity of the blood Thrombosis of blood inside the blood vessels may take place Acute Pulpitis Definition Acute inflammation of the pulp, which results from: progression of focal reversible pulpitis acute exacerbation of a chronic inflammatory process. Clinical features Reversible pulpitis Irreversible pulpitis Pain is short, sharp stabs Constant throbbing pain with sharp exacerbations Stimulated by hot and cold or osmotic (sweet) stimuli Spontaneous exacerbations, as well as hot and cold or osmotic (sweet) stimuli. In late stages cold may relieve the pain Pain persists several minutes or hours after an exacerbating stimulus Pain resolves after stimulus removed in seconds or a few minutes Acute Pulpitis The extreme pain is due to: The fact that in pulp inflammation, edema is confined in a rigid chamber of dentin and the pressure is greater than that in loose connective tissue. The products of inflammation such as histamine and serotonin, act upon the nerve endings to produce pain. Acute Pulpitis Histopathology Initial hyperaemia limited to the area immediately beneath the irritant. And inflammatory fluid exudates may be seen as vesicles between the cells. Infiltration of the pulp by acute inflammatory cells (neutrophils) which are directed toward the site of bacterial invasion. destruction of odontoblasts due to osmotic imbalance Acute pulpitis Interrupted odontoblastic layer Dilated blood vessels Polymorphoneuclear leukocytes Acute Pulpitis neutrophils VD blood vessels Focal reversible pulpitis versus acute pulpitis Acute Pulpitis Histopathology Abscess formation  A great number of neutrophils die releasing proteolytic enzymes which dissolve the pulp tissue (liquefaction necrosis) and resulting in the production of pus.  This way an abscess is formed which contains:  inflammatory cells  inflammatory exudate  microorganisms  tissue debris. Acute Pulpitis Histopathology Abscess formation  Abscess is localized by granulation tissue and chronic inflammatory cells (plasma cells and lymphocytes)  The first abscess is most commonly seen in pulp horn  Later, inflammation spreads, then liquefaction necrosis of the whole pulp follows (total suppurative pulpits). Acute Pulpitis Treatment Root canal treatment Definition Chronic Pulpitis It is a chronic inflammatory reaction of the pulp that may result from long-term, low-grade injury [When the irritant is not severe enough to cause acute infection] Examples  When organisms are of low virulence.  Slowly progressing caries.  May develop as a sequel of acute pulpitis  It may develop in normal teeth not affected by caries, through haematogenous ] infection (Anachoretic pulpitis). Chronic Pulpitis Reparative process Destructive changes Chronic pulpitis Chronic closed pulpitis Chronic open pulpitis Chronic open ulcerative pulpitis Chronic open hyperplastic pulpitis Chronic closed pulpitis Clinical Features The tooth may exhibit intermittent dull aching pain. Sensitivity to heat and cold is less than that in acute pulpitis [due to degeneration of nerve fibers] pain is poorly localized and may be felt in any of the teeth of the upper or lower jaw of the affected side (but never cross the midline). The tooth responds at a higher level to electric pulp tester than does the normal. Chronic closed pulpitis Histopathology As there is low-grade irritation so, considerable amounts of reactionary dentin continue to form, but inflammation progresses beneath it. Chronic closed pulpitis Histopathology  The pulp tissue shows: a. Chronic inflammation cells, (plasma cells, lymphocysts) b. Prominent blood capillaries. c. Collagen fibers (fibroblastic activity which is an attempt by the pulp to wall off the infection). Pulp death is the end result. Chronic Pulpitis Treatment Root canal treatment Chronic open pulpitis Chronic open ulcerative pulpitis Is a condition in which the pulp chamber is open to the oral cavity [large portions of the crown are usually missing] Chronic open hyperplastic pulpitis Chronic Open Ulcerative pulpitis Clinical features Symptoms range from non to a minimum, with slight irregular pain of a dull character made worse by thermal changes. Edema in the pulp [which causes pressure and chemical irritation to the nerve endings] escapes from the superficial part of the tissue through the exposure. So symptoms may be decreased or disappeared Chronic Open Ulcerative pulpitis Histopathology: pulp tissue is replaced by granulation tissue: 1. Dilated blood vessels 2. Collagen fiber bundles 3. Chronic inflammatory cells (lymphocytes, macrophages, plasma cells) Chronic Open Hyperplastic pulpitis (pulp polyp) It is a special form of chronic pulpitis that occurs in  The molar teeth (primary and permanent) of children and young adults.  The involved teeth exhibit large carious lesions that open into the coronal pulp chamber. Chronic Open Hyperplastic pulpitis (pulp polyp) The pulp tissue reacts in a hyperplastic manner, producing, a red mass of granulation tissue that extrudes through the pulp exposure.  This type of reaction is believed to be related to the wide apical foramen, through which a relatively rich blood supply flows. Chronic Open Hyperplastic pulpitis (pulp polyp) Clinical Features  Pulp polyp appears as a red or pinkish soft nodule protruding into the cavity.  It is painless (as there is no exudate under pressure) but may be tender and bleed on probing. Chronic Open Hyperplastic pulpitis (pulp polyp) Histopathology Pulp tissue is replaced by a well- vascularized granulation tissue mass. The deeper pulp tissue shows chronic inflammatory cells (plasma cells, lymphocytes) Chronic Open Hyperplastic pulpitis (pulp polyp) Histopathology Granulation tissue commonly gets covered by epithelium as a result of implantation of epithelial cells on its surface. Source of the epithelium: Desquamated epithelial cells of the oral cavity carried by saliva. Rubbing against buccal mucosa, tongue or gingiva. Pulp Necrosis Untreated pulpitis may lead to. Death of the pulp The inflammatory exudates compressed within hard shell of dentin Leads to compression of blood vessels Which then leads to infection and necrosis Pulp Necrosis Clinical features: Clinically, necrosis is characterized by cessation of all symptoms. Microscopically: Microscopic section shows either an empty pulp chamber and canals or isolated areas of necrotic structure-less masses. Key points The inflammatory process in the pulp is basically the same as elsewhere in the body connective tissue, however pulp anatomy has its own significance Main irritants of the pulp are either living irritants (microbial) or non living irritants (mechanical, chemical, electrical, thermal) Most commonly used classification of pulp inflammation depends on severity & duration, it comprises: focal reversible, acute and chronic pulpitis Pulpitis is reversible [level of pulp inflammation is capable to return to normal state if the irritant is removed] or irreversible [a higher level of inflammation in which dental pulp has been damaged beyond the point of recovery] Chronic pulpitis shows both reparative and destructive processes Aim: The aim of this lecture is to review the histopathological features of common pulpal disease Objectives: On completion of this lecture, the student should be able to: Understand the histopathological features of acute and chronic pulpal disease Understand the key cellular infiltrates of acute and chronic inflammation Pulpal Diseases Reading material: Students are advised to review any relevant teaching provided in the first year. In addition they are advised to read relevant sections of the following texts: Robinson M et al. Soames’ and Southam’s Oral Pathology. 5th edition. Oxford University Press, 2018 pp107-118 Odell E.W. Cawson’s Essentials of Oral Pathology and Oral Medicine. 9th Edition. Elsevier, 2017 pp 23-44 Thank you