Lecture 7: Disease of Periapical Tissue PDF

Disease of periapical tissue The periapical area: It means the area which surrounds the apical foramen of the dental root. The Periapical Lesions: It means the Inflammation surrounds the ap ical foramen of the dental root. Etiology of the periapical lesions: i.Pulpitis. ii.Traumatic injury. iii....

Disease of periapical tissue The periapical area: It means the area which surrounds the apical foramen of the dental root. The Periapical Lesions: It means the Inflammation surrounds the ap ical foramen of the dental root. Etiology of the periapical lesions: i.Pulpitis. ii.Traumatic injury. iii.Deep seated restorations. iv.Infection through the gingival crevice as periodontal diseases. v.Use of unsterilized instruments during the root canal treatment. vi.Application of strong chemical antiseptic during the root canal treatment.  Periapical Periodontitis It is inflammation of PDL around apical portion of root Types: 1)Acute periapical periodontitis 2)Chronic periapical periodontitis  Acute periapical periodontitis  It is painful inflammation of the periodontium as a result of trauma , or irritation or infection through the root canal, regardless of whether the pulp is vital or nonvital.  Also referred to as symptomatic apical periodontitis.  Tooth is tender on percussion & pain can be sever making closure of teeth difficult. Etiology Clinical feature: Hot or cold substances do not cause pain in the tooth. Slight extrusion of tooth from socket. Cause tenderness on mastication due on inflammatory edema collected in PDL. Due to external pressure , forcing of edema fluid against already sensitized nerve ending results in sever pain Clinical diagnosis : preapical test (tender to percussion ) Radiographical feature: Widening of PDL space Histopathological features: Acute apical periodontitis is a typical acute inflammatory reaction with engorged blood vessels and packing of the tissue with neutrophils. Inflammation is transient ,if caused by acute trauma. If irritant not removed , progress into surrounding bone resorption. Abscess formation may occur if it is associated with bacterial infection (acute preapical abscess \ alveolar abscess ) Treatment:  Selective grinding if inflammation due to occlusal trauma. Etraction & RCT be done to drain exudate. Acute apical periodontitis. In this early acute lesion inflammatory cells, mainly neutrophil polymorphonuclear leukocytes, are seen clustered around the apex of a non-vital tooth. The inflammatory cells are spreading around and into bone and there has not yet been time for significant bone resorption to develop.  Acute periapical abscess (Dentoalveolar abscess)  An acute suppurative process of the dental periapical region. It is the accumulation of acute inflammatory cell at apex of nonvital tooth. Etiology:  Infection: following pulpitis, or hematogenous spread.  Traumatic injury.  Pulp necrosis.  Mechanical/chemical manipulation in R.C.T.  More commonly, it is acute exacerbation originates in an area of chronic infection; e.g.: periapical granuloma (phoenix abscess). Abscess related to maxillary canine pointing buccally. Clinical Features: History of pain due to previous pulpitis. A large carious cavity or filling is usually present. Thermal stimulation doesn't cause pain because of pulp necrosis. When periodontitis develops, escape of exudate into PDL causes the tooth to be: Extremely painful. Extremely sensitive to percussion. Slightly extruded from its socket.  As pus starts to form, pain becomes intense & throbbing in character. Systemic manifestations At this stage, gingiva over the root is red & tender, no swelling as inflammation is confined within bone. Lymphadenitis and fever may be present Radiographic features: It appears as an amorphous radiolucent area with an irregular faintly m argin in the periapical area of the dental root Histopathological features: Abscesses show dense, almost solid masses of neutrophils (pus cells) often inter- mixed with inflammatory exudate, cellular debris, necrotic material, bacterial colonies, or histiocytes. dilated blood vessels in PDL & bone marrow space The bone marrow show inflammatory infiltration The surrounding bone shows resorption and degeneration of osteocytes. Complications of untreated periapical abscess: 1. Pus may discharge directly into oral cavity through a sinus track. This may occur with or without pain or swelling. A nodule of granulation tissue often forms and opening of sinus track- “gumboil” or “parulis”. 2. Pus which is tracking palatally may spread under the dense palatal mucoperiosteum, presenting as a palatal abscess. 3. Abscesses in molar regions may penetrate the buccal cortical plate above (maxilla) or below (mandible) attachments of buccinator muscle. Inflammatory edema and suppuration may spread into soft tissues of face or neck, presenting as cellulitis or as a localized soft tissue abscess. Such an abscess may discharge through a sinus on skin surface. 4. Abscesses related to anterior maxillary teeth may perforate bone above attachment of levator anguliorisms. Infectionthen passes medially and upwards towards inner canthus of eye and into lower eyelid. Alternatively, it may pass into upper lip. 5. Abscesses related to maxillary molars and premolars may discharge into the maxillary sinus. 6. Abscesses related to mandibular premolar or molar teeth may perforate lingual plate of mandible below mylohyoid muscle attachment to involve submandibular space which has communications with sublingual and lateral pharyngeal spaces  As infection erodes through bone , it can express itself in variety of places depending on thickness of overlying bone and relationship of muscle attachment to site of perforation. This illustration notes six possible locations : 1. Vestibular abscess 2. Buccal space 3. Sublingual space 4. Submandibular space 5. Maxillary sinus. A Palatal abscess related to lateral incisor. Treatment: It requires administration of antibiotic, analgesic Draing of abcess by opening the pulp chamber is performed, api cectomy or extraction. Localized extraoral spread of abscess related to a mandibular molar.  Cellulitis It is a diffuse inflammation of soft tissues which is not circumscribed of confined to one area , but which in contrary to the abscess ,tend to spread through tissue spaces and long fascial spaces. Clinically 1)Painful. 2)Swelling of the involved soft tissues. 3)usually associated with malaise and an elevated temperature. 4)trismus rather than facial swelling. 5)Much of the swelling is due to inflammatory edema, suppuration and abscess formation. 6)Extension of cellulitis associated with maxillary teeth towards the eye is a potentially serious complication. 7)Involvement of veins at inner canthus of eye may result in cavernous sinus thrombosis Etiology : Itoccurs as result of infection by microorganism that produce significant amount of streptokinase ,hyaluronidase and fibrinolysins which acts to breakdown or dissolve hyaluronic acid , the universal intercellular cement substance , and fibrin. Microorganisms include Veillonella sp.,Porphyromonas sp., Streptococcus sp., Fusobacterium sp. and Actinomyce Dental infection Sequela of periapical abscess or osteomyelitis Pericoronitis Tooth extraction or injection with infected needles Cellulitis associated with spread of inflammation from abscess related to a maxillary molar. Cavernous Sinus Thrombosis Etiology and pathogenesis Infection of maxillary premolar and molar teeth Infection from maxillary anterior teeth Symptoms: There is high spiking fever Signs: Signs of meningeal irritation including severe headache, stiffness of neck, ocular palsy and facial weakness Eye: Proptosis or protrusion of eye is seen as a result of decreased venous drainage, chemosis and edema of eyelid, which is secondary to venous stasis Ludwig angina Ludwig's angina is severe cellulitis involving the, usually as a result of initial involvement of the submsubmandibular, sublingual, and submental spaces. Clinical Features: Brawny induration: It is characterized by brawny indurations. Tissues are board-like and do not pit on pressure. No fluctuation is present Swelling of floor of mouth, elevated tongue, difficult eating, swallowing, & breathing. Open mouth and respiratory obstruction woody tongue Bull neck Treatment Maintenance of the airway Antibiotic high dose IV (Pen+ Metronidazole) Corticosteroid  Chronic periapical abscess Features: May arise as a chronic condition or as a sequela of acute infection. Clinically: No acute symptoms, but the tooth felt high in socket. Intra-oral sinus formation salty taste. Microscopically: Puscavity involves chronic inflammatory cells lymphocytes, plasma cells and macrophage. Fibrous tissues and newly formed capillaries, rarely PMNLs found. At the periphery, a well-formed fibrous capsule.  Chronic periapical periodontitis (or periapical granuloma) Periapical granuloma: It is a localized granulation tissue mass which surrounds the apical foramen of the non vital tooth. It is the most common periapical lesion Itis resulting from death of the pulp and the diffusion of bacterial toxins from the root canals into surrounding periradcular tissue through the apical and lateral canal. Presence of lateral or accessory root canal opening on the lateral surface of the root give rise to lateral granuloma Etiology: 1)Death of the pulp 2)Infection through the gingival crevice. 3)Trauma. 4)Haematogenous infection. 5)Odonto-iatrogenic. Clinical features 1)The tooth is non-vital. 2)May be slightly tender to percussion due to odema and inflammation of the apical periodontal ligament. 3) The symptoms may be minimal. 4) Mild pain when biting or chewing on solid food. 5)The involved tooth is slightly extruded from its socket. 6)Sensetivity is due hyperemia ,edema, &inflammation of PDL 7)In many cases asymptomatic 8)No perforation of bone & oral mucosa forming fistula tract unless undergoes acute exacerbation Radiographical features Thearea is usually about from 5 mm to1cm in diameter in diameter and has well-defined margins. Itappears as a rounded radiolucent area with regular demarcat ed margin surrounding the apical foramen of the dental root. Thin radiopaque line of sclerotic bone sometime seen outlining lesion Long standing lesion may show varying degree of root resorption. Histopathological features: Hyperemia and edema of the PDL Granulation tissue containing fibers, fibroblasts ,endothelium cell, chronic inflammatory cell infiltration and blood vessels. Granulation tissue is outlined by a capsule of fibrous tissue which are firmly attached to the cementum ,so that during extraction of the tooth is associated with this granuloma. Presence of foam cells which represent macrophages containing lipid materials. Presence of cholestrole crystals as empty clefts due to the processing of slides. Presence of epithelial islands (Epithelial rests of Malassez). Treatment: It requires apicectomy with root canal treatment. An apical granuloma showing neutrophils, lymphocytes and plasma cells in loose oedematous fibrous tissue. Complication of the periapical granuloma: Painless due to infected periapical granuloma. Periapical cysts develops due to proliferation of the epithelial rests of Malassez presenting in the histological structure of periapical granuloma. Cholesterol clefts with associated foreign-body giant cells. Histological section of root and attached periapical granuloma from Note the more heavily inflamed central area of the periapical granuloma (blue/purple stained), compared to the less inflamed, more collagenous peripheral zone.  Osteomyelitis It is an acute or chronic inflammatory process in the medullary spaces or cortical surfaces of bone that extends away from the initial site of involvement (usually a bacterial infection). Classification: 1- Acute Suppurative Osteomyelitis 2- Chronic Suppurative Osteomyelitis 3- Chronic Low-Grade Osteomyelitis and Osteitis (Sclerosing Osteomyelitis) 4- Focal sclerosing osteomyelitis (focal condensing osteitis) 5- Chronic Osteomyelitis with Proliferative Periostitis (Garré’s Osteomyelitis, Periostitis Ossificans) Etiology:  Most common cause : dental infection Infection due to fracture of jaw , gun shot wounds Hematogenous spread Predisposing factors : Radiation damage Paget’s disease Osteoporosis Systemic disease (malnutrition , acute leukemia, uncontrolled diabetes ,sickle cell anemia ,chronic alcoholism )  A) Acute osteomyelitis Acute Suppurative Osteomyelitis A rapidly destructive inflammatory process within bone and bone marrow due to virulent strain of bacteria. It used to be a common complication of dental infection before advent of antibiotics. Pathogenesis: Acute inflammatory process that spreads through the medullary spaces of the bone associated with virulent bacterial organism’s and\or reduced host’s immune resistance.  Pathology Acute inflammation of marrow tissue Spread of exudate along the marrow spaces Thrombosis of vessels due to compression Necrosis of bone Necrotic tissues ,dead and drying cell , pus from bacteria Fill the bone marrow Involves cortical bone Lifting of periosteum causing further necrosis Finally osteoclastic activity Clinical Features Sex: Most patients are adult males with infection of the mandible. Site : The mandible is much more frequently involved than the maxilla Sign, symptoms: Early complaints: A severe, throbbing, deep-seated pain. Swelling of affected area External swelling due to inflammatory edema. Later, distension of the periosteum with pus. Finally, subperiosteal bone formation causes the swelling to become firm. The overlying gingiva is red, swollen and tender. Associatedteeth are tender; they may become loose, and pus may exude from an open socket or gingival margins. Muscle edema causes difficulty in opening the mouth and swallowing. Regional lymph nodes are enlarged and tender. Anesthesia or paresthesia of the lower lip is characteristic. Radiographic changes: Appear after at least 10 days. Loss of trabecular pattern and areas of radiolucency indicate bone destruction. These areas have ill-defined margins Histological features: A purulent exudate occupies the marrow spaces in acute osteomyelitis. Bony trabeculae show reduced osteoblastic activity and increased osteoclastic resorption with a loss of osteocytes. Ifan area of bone necrosis occurs (sequestrum), osteocytes are lost and the marrow undergoes Showing non-vital bone (the liquefaction. osteocyte lacunae are empty) and bacterial colonization, and acute inflammatory cell infil eroded outline with tration ( neutrophils). superficial lacunae, produced by osteoclastic resorption, and a dense surface growth of bacteria.  B) Chronic osteomyelitis 1-Chronic Suppurative Osteomyelitis Etiology: 1-sequelae of acute osteomyelitis: 2- Long term, low grade inflammatory reaction. Pathogenesis: Chronic osteomyelitis is commoner than acute osteomyelitis. Persistentlow-grade infection is associated with bone destruction and granulation tissue formation, but little suppuration. There are similar predisposing factors, but local bone sclerosis is much more likely for chronic osteomyelitis. Clinical feature: The most common site is the posterior area of the mandible. Low-grade pain Bad taste from pus draining to the mouth through sinuses. In more active phases there is swelling, increased pain and discharge, and increased tooth mobility. It shows irregular, ill defined. Histopathological features: It consists of chronically inflamed fibrous connective tissue filling the intertrabecular area of the bone with scattered sequestra.  Chronic Low-Grade Osteomyelitis and Osteitis (Sclerosing Osteomyelitis) osteomyelitis is so small or caused by such low virulence organisms that the clinical presentation is dominated by the local bone reaction to the infection rather than the infection itself. Suppuration and infiltration of marrow spaces by inflammatory cells are absent and bacteria are not readily cultivable. Types: 1. Diffuse sclerosing osteomyelitis was noted earlier. 2. Focal sclerosing osteomyelitis. 3. Proliferative periostitis  Diffuse sclerosing osteomyelitis Diffuse bone reaction to low grade inflammatory stimulus. Pathogenesis: Chronic intra-bony mild bacterial infection creates mass of chronically inflamed granulation tissue that stimulates sclerosis of the surrounding bone. 1-Dense mass of sclerotic bone trabeculae. 2- Fibrotic marrow tissue. Bone marrow infiltrated with a small number of lymphocytes & plasma cells. Clinical feature: Adults affected. Mandible affected. Usually asymptomatic. Bony swelling. Radiograph: It reveals Ill-defined diffuse radiopaque area affecting a large part of the jaw.  Focal sclerosing osteomyelitis (Focal condensing osteitis) It is a Focal bony reaction to low-grade periapical infection, or pulpal inflammation, or unusually strong host defensive response. Clinical feature: Children and young adults affected. Premolar or molar region of mandible affected. Usually asymptomatic. No expansion of the jaw. Radiographic picture: Localized but uniform radiodensity (radiopaque) related to tooth with widened periodontal ligament space or periapical area. Pathology Result from low grade irritation, or/and high tissue resistance in children that stimulate: 1- Dense mass of sclerotic bone trabeculae. 2- Scanty fibrotic marrow tissue. 3- Infiltrated with a small number of lymphocytes & plasma cells.  Chronic Osteomyelitis with Proliferative Periostitis (Garré’s Osteomyelitis, Periostitis Ossificans)  It is characterized by formation of hard bony swelling at the periphery of the jaw. It is essentially a periosteal osteosclerosis  The affected periosteum forms several rows of reactive vital bone that parallel each other and expand the surface of the altered bone.  Affected patients tend to be primarily children and young adults, with a mean age of 13 years.  No sex predominance is noted.  Vague pain and prominent bony enlargement. Mandible related to lower first molar. Radiograph: Occlusal radiograph shows duplication of the cortex “onion skin” appearance. Histopathology:  A supra-cortical but subperiosteal mass composed of parallel layers of reactive new bone or osteoid with osteoblasts bordering many of the bony trabeculae.  The connective tissue between bony trabeculae is fibrous and shows diffuse or patchy collections of lymphocytes and plasma cells.  Small sequestra if present.