Periapical Infection Group 3 PDF

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Malak Khaled, Dalya Omar, Fadilah Ahmed, Shouq Hassan

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dental pulpitis periodontitis dental procedures

Summary

This document provides an overview of periapical infection, including the causes, symptoms, and management strategies for this dental condition. It includes information on different types of pulpitis and the related pathologies.

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PERIAPICAL INFECTION By: Malak Khaled Dalya Omar Fadilah Ahmed Shouq Hassan Contents:  Pathology  Causes & Symptoms  Treatment and Management in Dental Practice Pulpitis Pulpitis is painful inflammation of the tooth pulp caused by invasion o...

PERIAPICAL INFECTION By: Malak Khaled Dalya Omar Fadilah Ahmed Shouq Hassan Contents:  Pathology  Causes & Symptoms  Treatment and Management in Dental Practice Pulpitis Pulpitis is painful inflammation of the tooth pulp caused by invasion of bacteria leading to swelling of the pulp. Causes of pulpitis Dental caries Traumatic exposure of the pulp Fracture of a crown or cusp Cracked tooth Thermal or chemical irritation Types of Pulpitis Acute Pulpitis Chronic Pulpitis In the early stages the tooth is Chronic pulpitis may develop hypersensitive. Very cold or hot with or without episodes of food causes a stab of pain that stops as soon as the irritant is acute pulpitis. However, many removed. While inflammation pulps under large carious progresses, pain becomes cavities die painlessly. The first more persistent after the indication is then develop- stimulus, and there may be prolonged attacks of ment of periapical periodontitis, toothache. The pain may start either with pain or seen by spontaneously, often when the chance in a radiograph. In patient is trying to get to sleep. other cases, there are bouts of The pain is partly due to the pressure on the irritated nerve dull pain, brought on by hot or endings from oedema within cold stimuli or occurring the rigid pulp chamber and spontaneously. There are often partly due to release of pain- prolonged remissions, and there producing mediators from the damaged tissue and may be recurrent acute inflammatory cells. Although exacerbations. pulp death is the likely outcome, acute pulpitis may progress to chronic pulpitis, and early treatment can still preserve pulp vitality. Pathology  Pulpitis caused by early caries results from penetration of acid and bacterial products through the dentine, and later from a mixed bacterial infection penetrating to the pulp. Acute closed pulpitis refers to inflamation inside an intact closed pulp chamber. Histologically, there is initial hyperaemia limited to the area immediately beneath the irritant.Infiltration by inflammatory cells and destruction of odontoblasts and adjacent pulp follow. A limited area of necrosis may result in formation of an abscess, localised by granulation tissue. Chronic closed pulpitis The main features are a pre- dominantly mononuclear cell infiltrate and inflammation more limited in extent. A small area of pulpal necrosis and pus formation may be localised by a well-defined wall of granulation tissue, and a minute abscess may thus form. The remainder of the pulp may still appear normal.  Chronic hyperplastic pulpitis (pulp polyp) In this rare condition, despite wide pulpal exposure, the pulp not merely survives but proliferates through the opening to form a pulp polyp. It is painless but may be tender and bleed on probing. When a pulp polyp forms, the pulp itself becomes replaced by granulation tissue. Symptoms of Pulpitis Pulpitis causes intense tooth pain. If an abscess is present, the tooth becomes extremely sensitive to pressure and tapping with a dental instrument Management If fractured or cracked, stabilise fracture and seal pulp temporarily Removal of caries, obtundent or steroid dressing Removal of caries and pulp capping Pulpotomy in deciduous teeth Endodontic treatment Extraction Analgesics are largely ineffective Apical periodontitis Apical periodontitis is the local inflammation of the periapical tissues that originate from pulp disease. It may occur due to the advancement of dental caries, trauma, or operative dental procedures. The infected pulp is the main cause of apical periodontitis. Clinical features  Acute Apical Periodontitis Spread of infection through the apex brings the causative bacteria from a protected site into an environment where the host can mount an effective host response. Acute inflammation and an immune reaction are triggered. The patient may give a history of pain due to previous pulpitis, and the associated tooth may be carious, restored or discoloured due to death of the pulp. Formation of inflammatory exudate in the periodontal ligament causes the tooth to be extruded by a minute amount and the bite to fall more heavily on it. The tooth is at first uncomfortable, then increasingly tender, even to mere touch. Hot or cold substances do not cause pain in the tooth unless some viable pulp remains, as it may in a multirooted tooth. Radiographs may show immediately around the apex, the lamina dura appearing slightly hazy and the periodontal space may be slightly widened. Diagnosis Clinical Examination: Apical periodontitis often presents with symptoms like tenderness, swelling, or pain upon biting. Dentists also check for mobility and tenderness to palpation Radiographic Assessment:detect periapical radiolucency Pulp Testing**: Dentists often use thermal or electric pulp testing to assess the vitality of the tooth Treatment Options Non-surgical Root Canal Therapy (RCT) Apicoectomy Periapical curettage *Antibiotics and Pain Management(Antibiotics should not be given for simple acute periodontitis if immediate dental treatment is available) Dentoalveolar abscess A dentoalveolar abscess also known as Periapical abscess is an acute lesion characterized by localization of pus and acute inflammatory cells at the apex of nonvital tooth. Causes of dentoalveolar abscess -Commonly a result of acute apical periodontistis(the case when the diseased tissue undergoes suppuration -Deep caries Trauma -Failed dental procedure Clinical Features & Radiographic Features  Periapical abscesses are designated as symptomatic or asymptomatic on the basis of their clinical presentations.  Periapical abscesses become symptomatic as the purulent material accumulates within the alveolus. The initial stages produce tenderness of the affected tooth that often is relieved by direct application of pressure. With progression, the pain becomes more intense, often with extreme sensitivity to per- cussion, extrusion of the tooth, and swelling of the tissues. The offending tooth does not respond to cold or electric pulp testing. Headache, malaise, fever, and chills may be present.  Radiographically, abscesses may demonstrate a thickening of the apical periodontal ligament, an ill-defined radiolu- cency, or both. Pathology  May develop either directly from acute periapical periodontitis or from a chronic periapical granuloma.  After the initial infection,and as the disease progresses, the pulp dies, the bacterial infection spreads into the periapical tissues,the body responds by sending white blood cells (neutrophils and macrophages) to the area to fight the infection. This leads to the formation of pus, which is a combination of dead cells, bacteria, and tissue debris. - The pus builds up, creating a periapical abscess at the tip of the tooth root.  The infection is usually polymicrobial dominated by anaerobic bacteria such as;Porphyromonas spp,Prevotella, Fusobacterium nucleatum.  Complications;If the pus cannot drain, it leads to increased pressure and pain. - The infection can extend into surrounding alveolar bone, leading to localized destruction and the formation of a bone cavity filled with pus. the infection can extend to the surrounding tissues, including the bone (osteomyelitis), soft tissues (cellulitis), and even spread systemically, leading to sepsis. Symptoms, & Management Symptoms  Management -Sharp pain,usually severe Drain the abscess(via incision) -Redness in the mouth RCT -Sensitvity in the affected area -Bad taste in the mouth Extraction -Difficulty in chewing Antibiotics -High temperature Pain killers -Swollen face or jaw Apical granuloma Localized mass of chronic granulation tissue at the apex of root of a non-vital tooth as a response to infection. Causes: -It is commonly a result of chronic periapical periodontitis -Physical trauma to pulp causing pulp necrosis -Chemical irritation -Failed RCT Pathology Periapical granulomas may arise after quiescence of a periapical abscess or may develop as the initial periapical pathosis. Pulpal Necrosis: Apical granuloma typically forms after the pulp becomes necrotic due to bacterial infection, trauma, or severe decay. Once the pulp dies, bacteria and their byproducts migrate through the root canal and into the periapical tissues, initiating an immune response. Chronic Irritation: The continual presence of bacteria, toxins, and necrotic tissue at the root apex causes persistent inflammation. This chronic irritation is the primary driver of granuloma formation. Histopatholgy -Granulation tissue attached to the root Immune and Inflammatory Response apex Inflammatory Cells: Chronic inflammation around the tooth root -Mixed inflammatory cells ,cholesterol leads to the recruitment of various immune cells, including clefts & Russel bodies may be seen macrophages, lymphocytes, and plasma cells. These cells try to eliminate the bacterial infection and wall off the area. In response -Epithelial rest of Malassez may be present to this persistent inflammation, fibroblasts are activated and start producing collagen, which forms a fibrous capsule around the infection site. This forms the granuloma tissue.The hallmark of an apical granuloma is the presence of granulation tissue at the apex of the tooth. Clinically:Most periapical granulomas are asymptomatic, but pain and sensitivity can develop if acute exacerbation occurs. Typically, the involved tooth does not demonstrate mobility or significant sensitivity to percussion. The soft tissue over- lying the apex may or may not be tender. The tooth does not respond to thermal or electric pulp tests unless the pulpal necrosis is limited to a single canal in a multirooted tooth. Radiographically:The associated radiolucencies are variable, ranging from small, barely perceptible lesions to lucencies exceeding 2 cm in diameter. Affected teeth typically reveal loss of the apical lamina dura. The lesion may be circumscribed or ill- defined and may or may not demonstrate a surrounding radiopaque rim. Root resorption is not uncommon Diagnosis Granuloma is discovered in many cases with an X-ray that shows a dark, usually roundish area of the bone surrounding the root. TREATMENT A granuloma can remain silent for years and flare up due to an increased bacterial load. In this case, antibiotic therapy combined with root canal treatment of the affected tooth is indicated. Apicoectomy Extraction Apical cysts Apical cysts, also known as radicular cysts, Is the most common epithelial lined odontogenic cyst of inflammatory origin that develop in a non vital tooth. Causes: -Commonly due to progression of a dental granuloma -Caries -Periodontal disease -Trauma -Complications from a previous RCT -Periapical osteitis -Bacterial infections Radicular cysts are subdivided into apical, lateral, and residual types depending on the anatomical relationship of the cyst to the root of the tooth Apical cyst Lateral cyst Residual cyst (The most common) Appear as discrete The residual periapical cyst radiolucencies along the lateral appears as a round-to-oval aspect of the root. radiolucency of variable size within the alveolar ridge Pathology Histopathology  Pathogenesis Initial Infection: The process -Non keratinized lining typically begins with pulp necrosis, often caused by untreated dental caries or epithelium of variable trauma, leading to bacterial invasion of the thickness root canal system. Spread of Infection: The -Arcading patterns of infection spreads beyond the confines of the tooth’s root into the surrounding periapical epithelium tissues. Chronic Inflammation: Persistent -Dense inflammation of inflammation leads to the formation of granulation tissue at the root apex, which cystic capsule triggers a response from the surrounding -Cholestrol clefts bone and soft tissues. Epithelial Proliferation: The epithelial cell rests of Malassez, remnants of the dental lamina, proliferate in response to inflammation. This proliferation forms the lining of the cyst. Cyst Formation: As epithelial cells continue to proliferate, a cystic cavity forms. Inside the cyst, fluid accumulates, creating a well- circumscribed cavity filled with necrotic debris and inflammatory cells Diagnosis -Clinical examination -Radiographic imaging -(some cases CBCT) -Biopsy Treatment The main treatments to remove a periapical cyst are: Surgery. Endodontic treatment. Antibiotic treatment. Condensing osteitis Localized areas of bone sclerosis associated with the apices of teeth with pulpitis (from large carious lesions or deep coronal restorations) or pulpal necrosis are termed condensing osteitis. Causes: Usually arises from chronic,low-grade inflammation,often due to infected or necrotic dental pulp,typically in the molar & premolar regions. Symptoms: May or may not present with symptoms.Some pateints experience mild or discomfort,but others may be asymptomatic and the condition is discovered incidentally during routine dental X-rays. Treatment  Treatment of the patient with condensing osteitis consists of res- olution of the odontogenic focus of infection. After extraction or appropriate endodontic therapy of the involved tooth, approx- imately 85% of cases of condensing osteitis will regress, either partially or totally. Typically, resolution of the lesion is associ- ated with normalization of the associated periodontal mem- brane. If the lesion persists and the periodontal membrane remains wide, then reevaluation of the endodontic therapy should be considered. A residual area of condensing osteitis that remains after resolution of the inflammatory focus is termed a bone scar Proliferative periostitis Bone formation within a periosteal reaction is a common finding that occurs in a wide variety of intraosseous pathoses and in all age groups. Causes of periosteal new bone formation include osteomyelitis, trauma, cysts, infantile cortical hyperostosis, fluorosis, avitaminosis C, hypertrophic osteoar- thropathy, congenital syphilis, and neoplasms (such as, Ewing sarcoma, Langerhans cell histiocytosis, and osteogenic sarcoma). Of these, osteomyelitis and malignant neoplasms are associated most frequently with formation of bone within a periosteal reaction. Clinical & Radiographic features  Affected patients tend to be primarily children and young adults, with a mean age of 13 years. No sex predominance is noted. As expected, the most frequent cause is dental caries with associated periapical inflammatory disease, although lesions have been reported secondary to periodontal infections, pericoronitis, tooth extractions, fractures, buccal bifurcation cysts, and non-odontogenic infections. Examples adjacent to an uner- upted developing tooth also have been documented.Most cases arise in the premolar and molar area of the mandible. The hyperplasia is located most frequently along the lower border of the mandible.  Appropriate radiographs demonstrate radiopaque laminations of bone that roughly parallel each other and the under- lying cortical surface.The laminations vary from 1 to 12 in number, and radiolucent separations often are present between the new bone and the original cortex. Less frequently, the new bone formation exhibits consolidation and contains numerous fine bony projections that radiate perpendicular from the underlying and intact periosteum TREATMENT Unusually removal of the infected tooth Curettage of the socket are curative. Surgery should be done only if there is obvious facial asymmetry after at least a 6- month waiting period

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