Infections of the Jaws PDF

Infections of the jaws Chapter 8 Cawson’s Dr. Omar Omran Dr. Hasnaa’ Makkawi Tooth extraction  Immediate reaction after extraction Normal clotting mechanisms produce a loose clot that fills the bony and soft tissue socket shrinks below the level of...

Infections of the jaws Chapter 8 Cawson’s Dr. Omar Omran Dr. Hasnaa’ Makkawi Tooth extraction  Immediate reaction after extraction Normal clotting mechanisms produce a loose clot that fills the bony and soft tissue socket shrinks below the level of the adjacent soft tissues, pulling any mobile soft tissue inward to reduce the area of the clot exposed. Clot retraction is usually complete in 4 hours, and the surface of the clot changes from shiny to matt. After retraction, the clot continues to stabilize by fibrin cross-linking, so avoiding rinsing is usually recommended for 24 hours 2 days Lysis of the clot begins, caused primarily by the fibrinolytic enzyme plasmin, generated by activation of plasminogen in the clot. The ligament is still sharply defined emigration of inflammatory cells into the clot would be seen. the risk of dry socket from clot lysis or loss is highest----- the clot is not well anchored to the wall  4 days capillaries and fibroblasts (granulation tissue) are growing into the blood clot from the periphery so that it is now firmly fixed to the socket wall. Macrophages migrate into the clot and start to demolish it ready for replacement by granulation tissue. The surface of the clot is white and porous bacteria in the superficial fibrin, which gradually disintegrates. Epithelial hyperplasia at the gingival margin starts to grow over the intact clot, below the surface debris  8 days The socket is filled by granulation tissue and the superficial layers contain inflammatory cells. The granulation tissue is soft or gelatinous and contains little collagen. The periodontal ligament is no longer clearly identifiable. The lamina dura of the socket is intact. Epithelial migration is complete between 7 and 10 days.  18 days The socket is filled by granulation tissue and the fibroblasts within it have laid down a collagen network. The lamina dura is still visible. Woven bone is forming around the periphery of the socket. 6 weeks The woven bone has filled the socket and is remodeling to lamellar bone. The outline of the lamina dura persists for a very variable length of time. By 3 months, it is usually not detectable radiographically, but socket outlines may persist for years in the elderly  ALVEOLAR OSTEITIS (dry socket) By far the most frequent painful complication of extractions It is not really an infection but leads to superficial bacterial contamination of exposed bone and can progress to osteomyelitis, Osteitis simply means inflamed bone, not infection. Develops after 1%–2% of extractions, Lower-third molar extractions Unpredictable Etiological factors Excessive extraction trauma Limited local blood supply Gingival infection such as acute ulcerative gingivitis, pericoronitis or abscess Local anesthesia with vasoconstrictor Smoking Oral contraceptives Osteosclerotic disease: Paget’s disease, cemento-osseous dysplasia Radiotherapy History of previous dry socket  The immediate cause is early loss of clot from the extraction socket due to excessive local fibrinolytic activity by fibrinolysin activators (plasmin), that are released when the bone is traumatized, degrading the clot and leaving the socket empty. The necrotic bone and socket lodge bacteria which proliferate freely in the avascular spaces unhindered by host defenses. In the surrounding tissue, inflammation prevents spread of infection beyond the socket walls. Dead bone is gradually separated by osteoclasts, sequestrate are usually shed in tiny fragments. bacterial colonization from the mouth is inevitable, and bacterial enzymes contribute to clot lysis  The appearance of an empty socket and exposed bone is diagnostic. When debris is washed, whitish dead bone may be seen or may be felt as a rough area with a probe and probing is painful. Sometimes the socket becomes concealed by granulations growing in from the gingival margins, narrowing the opening and trapping food debris. Pain often continues for a week or two, or occasionally longer. Sequestration of the socket wall may sometimes be seen radiographically  Healing is slow. Granulation tissue cannot grow in from the socket walls and base until the necrotic bone is removed. Although there is no infection within the tissues, the colonization of the socket and sequestrate by oral bacteria probably contributes to pain and slow healing. Anaerobes are thought to be significant and can produce fibrinolytic enzymes. antibiotics including metronidazole have not been shown to either prevent dry socket or speed healing reliably. chlorhexidine rinsing preoperatively has been shown to reduce incidence.  Prevention of dry socket Preoperative infection control Scaling teeth before extraction Chlorhexidine rinsing preoperatively and for 3 days postoperatively Atraumatic extraction Adherence to postoperative instructions No rinsing or forceful spitting No hot fluids No smoking Postoperative antibiotics only for those at particular risk  Treatment Keep the open socket clean Protect exposed bone from excessive bacterial contamination. The socket should be irrigated with mild warm antiseptic or saline to remove all food debris Minimum placing a dressing into the socket to deliver analgesia and close the opening so that further food debris cannot enter the socket. Many socket dressings have been formulated and should be antiseptic, obtundent, adhere to the socket wall, and be absorbable. A dressing may only last 1–2 days, and the whole process needs repeating until pain subsides, normally after one or two dressings. Frequent hot saline mouthwashes also help keep the socket free from debris.  Cancer or have sclerotic bone disease-----postoperative antibiotic cover. Prevent osteomyelitis rather than dry socket. General anesthesia for a few patients that developed dry socket under local anesthesia including regional blocks. It is important to explain to patients that they may have a week or more of discomfort.  OSTEOMYELITIS OF THE JAWS Bacteria and inflammation spread through the medullary bone from a focus of infection. Local origin and not caused by blood-borne infection. Can be divided into suppurative and sclerosing osteomyelitis.  Suppurative osteomyelitis Onset of the 4 weeks disease Chronic osteomyelitis Acute osteomyelitis Deep bacterial invasion into medullary & cortical bone  Acute osteomyelitis of the jaws: potential sources of infection Periapical infection Pericoronitis Fracture through periodontal pocket or open to the mouth Acute necrotizing gingivitis in noma (also known as gangrenous stomatitis or cancrum oris) Penetrating, contaminated injuries (open fractures or gunshot wounds)  Factors predisposing to osteomyelitis Focal factors Systemic factors (decreased vascularity/ vitality of bone) (impaired host defense) trauma Immune deficiency /suppression radiation DM/ malnutrition Paget’s age Osteoporosis major vascular disease Important predisposing conditions for osteomyelitis Local damage disease of the jaws Radiation damage Causes of osteosclerosis Paget’s disease Fibro-osseous lesions, cemento-osseous dysplasia Osteopetrosis Impaired immune defenses Poorly controlled diabetes mellitus Sickle cell anemia Chronic alcoholism or malnutrition Drug abuse Tobacco smoking Malignant neoplasms and their treatment Clinical features Males Mandible Early: severe, throbbing, deep-seated pain swelling with external swelling due to inflammatory edema. The overlying gingiva and mucosa is red, swollen and tender. Later, distension of the periosteum pus may exude from an open socket or gingival margin Associated teeth are tender & loose Final: subperiosteal bone formation cause the swelling to become firm. Difficulty in opening the mouth and swallowing (muscle edema). Regional lymph nodes are enlarged and tender. Anesthesia or paranesthesia of the lower lip, caused by pressure on the inferior dental nerve, is characteristic. Acute phase, there may be fever and leukocytosis. Radiography Changes do not appear until after at least 10 days Loss of trabecular pattern and areas of radiolucency indicating bone destruction Widening of periodontal ligament. Areas of dead bone appear as relatively dense areas which become more sharply defined as they are progressively separated as sequestra.  ill-defined margins and a moth-eaten appearance similar to a malignant neoplasm. Later, in young persons particularly, subperiosteal new bone formation causes a buccal swelling and appears as a thin, curved strip of new bone below the lower border of the jaw in lateral or panoramic radiographs.  Osteomyelitis of the newborn is a distinctive variant. Affecting the maxilla shortly after birth. Potentially fatal. The cause is either birth injuries or uncontrolled middle ear infection.  Pathology Acute osteomyelitis is a suppurative infection with a mixed bacterial flora, much of which forms a biofilm on sequestra of bone. Oral bacteria, particularly anaerobes such as Bacteroides, Porphyromonas or Prevotella species, are important causes. Staphylococci may be responsible when osteomyelitis follows an open fracture and the bacteria enter from the skin. The mandible has a relatively limited blood supply and dense bone with thick cortical plates.  Infection and acute inflammation cannot escape, and the pressure spreads infection through the marrow spaces. It also compresses blood vessels confined within the rigid boundaries of the vascular canals. Thrombosis and obstruction then lead to further bone necrosis. Dead bone is recognizable microscopically by lacunae empty of osteocytes and medullary spaces filled with neutrophils and colonies of bacteria that proliferate in the dead tissue  Pus, formed by liquefaction of necrotic soft tissue and inflammatory cells, is forced along the medulla and eventually penetrates the cortex to reach the subperiosteal region by resorption of bone. Distension of the periosteum by pus stimulates subperiosteal bone formation, perforation of the periosteum by pus and formation of sinuses on the skin or oral mucosa.  At the boundaries between infected and healthy tissue, osteoclasts sequestrate the necrotic bones Once infection starts to localize, new bone forms around it, particularly subperiosteally. healing is by granulation tissue with formation of woven bone in the proliferating connective tissue. After resolution, woven bone is gradually replaced by compact bone and remodeled to restore normal morphology. Pathogenesis Organisms entry into the jaw, mostly mandible compromising vascular supply Medullary infections spreads through marrow spaces Thrombosis in vessels leading to extensive necrosis of bone Lacunae empty of osteocytes but filled with pus, proliferate in the dead bone Suppurative inflammation extend through the cortical bone to involve the periosteum Sequestrum is formed bathed in pus, separated from surrounding vital bone Summary of management of acute osteomyelitis Bacterial sampling and culture Vigorous (empirical) antibiotic treatment Drainage Analgesics Give specific antibiotics once culture and sensitivities are available Debridement Remove source of infection, if possible Adjunctive treatment Sequestrectomy: Dead bone should not be forcibly separated, Decortication if necessary hyperbaric oxygen Resection and reconstruction for extensive bone destruction  Vigorous (empirical) antibiotic treatment (Initially, penicillin, 600–1200 mg daily can be given by injection (if the patient is not allergic), with metronidazole 200–400 mg every 8 hours. Clindamycin penetrates avascular tissue better and is frequently effective. The regimen is adjusted later in the light of the bacteriological findings) Debridement: Local analgesia is usually impossible in the presence of acute infection, but the earlier any causative tooth can be removed the better. Drainage may be achievable through the root canal as a temporary measure. If so, it may be possible to retain and restore the tooth at a later date. Alternatively bur holes through the cortex or decortication, complications Pathological fracture extensive bone destruction Chronic osteomyelitis inadequate treatment Cellulitis spread of virulent bacteria Septicemia immune compromised  CHRONIC OSTEOMYELITIS ➔ much more common than acute osteomyelitis and arises from infection by weakly virulent bacteria or in avascular bone develop without a prior acute phase rarely does acute osteomyelitis lead to chronic osteomyelitis local bone sclerosis or irradiation are factors much more likely to predispose to chronic osteomyelitis than acute  Clinical features Persistent ache or pain, often relapsing. Bad taste from pus draining to the mouth through sinuses. Swelling, increased pain and discharge, Increased tooth mobility. There may be exposed bone. Initially the original focus of infection can be identified, but chronic osteomyelitis may persist after its removal and the chronic infection becomes self-perpetuating in the bone  Radiology Radiographic appearances are variable Patchy and poorly defined radiolucency and sclerosis, sometimes resembling a malignant neoplasm. Often contains radiopacities sequestra may be identified, and there may be a periosteal new bone layer