Pulp Diseases, Periapical Lesions & Osteomyelitis PDF

Pulp diseases The following part of pulp diseases deals with inflammatory presentations resulted mainly from irritating stimuli. These are the proposed etiology of pulp diseases: 1-mainly dental caries (direct microbial attack or their toxins), 2-cracked teeth or excessive trauma, 3-exposure durin...

Pulp diseases The following part of pulp diseases deals with inflammatory presentations resulted mainly from irritating stimuli. These are the proposed etiology of pulp diseases: 1-mainly dental caries (direct microbial attack or their toxins), 2-cracked teeth or excessive trauma, 3-exposure during cavity preparation, 4-bruxism and abrasion or friction, 5-thermal, 6-chemical, 7-electric or galvanic effect, 8- anachoretic pulpitis, and 9-aerodontalgia. Pulp irritation during or after operative procedures (iatrogenic), may result from: **Heat generated by rotatory instruments. **Some irritating ingredients of various disinfecting, capping or restorative materials. **Thermal changes conducted by metallic filling materials in deep cavities without effective lining. **Forces transmitted to the dentin during filling the restorative materials. **Galvanic shock of dissimilar metals in adjacent or opposing teeth. * Classification of pulp diseases: *Ingress of harmful products and / or bacteria through microleakage (dentinal tubules). 1- Pulp hyperaemia: the only reversible condition of pulpitis. 2- Acute pulpitis (focal or generalized), and acute pulp abscess. 3- Chronic pulpitis (focal or generalized), and chronic pulp abscess. 4- Chronic open pulpitis or pulp polyp (ulcerative or epithelialized). 5- Pulp necrosis, where inflammatory exudates or infection (micro-organisms) may spread to the periapical area. Dental caries--------˃Reversible pulpitis------˃Acute pulpitis and (Acute abscess)-----------˃Chronic pulpitis and (Chronic abscess) -------˃ Hyperplastic pulpitis------------˃Necrosis. 1-Pulp hyperemia (reversible pulpitis): Pain threshold is low, intensified with heat or cold (Why??), and electric stimuli. Pain is mild/ moderate, intermittent and lasts for 5-10". **Removal of the stimulus would result in recovery of the condition. Histologically: dilated vessels, edema of the surrounding tissue and odontoblasts (tissue still vital), due to plasma extravasation. 1 2-a-Acute pulpitis (focal or generalized): -It may start as an acute state or due to an acute exacerbation of a chronic one. Pain is referred to another nearby location (or the whole side, WHY?). Pain threshold is low. Pain is more persistent, with prolonged attacks (lasting more than 20", may start spontaneously, and often when the patient is sleeping (i.e. on recumbent position). -Pain is severe, sharp and stabbing in character. Pain is intensified with sweet foods, heat or cold application. Histologically: engorgement of the dilated vessels with Diffuse PMNLs infiltrate. Note: no RBCs, and extravasation of PMNLs to the surrounding odontoblasts. area (localized or generalized pulpitis). 2-b- Acute pulp abscess: It is localization of dead inflammatory exudate and cells. Pain becomes more intensified described as lancinating, continuous and increased with sweet foods, hot and cold application and on recumbent position.-Pain threshold is low. Histologically: Centrally localized necrotic tissue( purulent exudate), of micro-organisms, necrotic pulp tissue(debris), fibrin, RBCs ,surrounded by PMNLs, dilated& engorged vessels, few lymphocytes, plasma cells and macrophages. The outermost margin is formed of granulation Acute abscess due to pulp exposure, surrounded by tissue. PMNLs and localized by granulation tissue. 3-Chronic closed pulpitis:-Long standing, low grade stimulus may lead to the condition, or due to high tissue resistance, or quiescence of an acute state. Pain is dull, deep, mild, lasts longer and intermittent. Pain threshold is increased. Histologically: The pulp is infiltrated with mononuclear leukocytes, i.e. lymphocytes, plasma cells and macrophages. The surrounding tissue is formed of collagen fibers, newly formed capillaries, and chronic inflammatory cells (granulation tissue). **Chronic abscess: localization of chronic inflammatory cells with central necrotic mass, and surrounded by granulation tissue. 2 4- Chronic open pulpitis ( pulp polyp, chronic hyperplastic pulpitis): (Ulcerative or epithelialized).D.D. gingival polyp. It results due to large exposed carious lesions, and open apical foramens, i.e. deciduous & permanent molars of young patients. Mild stimulus so inflammation is not confined to solid, rigid area, with abundant vascularity. Mild pain or painless (due to reduction of nerve fibers). Histologically: -Granulation tissue. The surface is covered by either acute or chronic inflammatory cells (ulcerative open pulpitis), or covered by squamous epithelium (auto- transplantation of epithelial cells, from where?), called epithelialized pulp polyp.-This tissue usually protrudes from the tooth, of normal or faint color either due to less vascularity or epithelial covering. The gingival polyp is more sensitive???? and hemorrhagic???? 5- Pulp necrosis: -Is death of pulp tissue, i.e. no Referred pain???? The patient, in most cases, pain, non-vital tooth. There is no tissue or only can not localize the affected tooth, WHY? remains of dead tissues. 3  Periapical lesions and osteomyelitis This part deals with the inflammatory processes at the apical region of the teeth. When a stimulus reaches the apical area, the same sequence of inflammatory response takes place as discussed in inflammatory pulp diseases. i.e. 1-hyperemia, 2-acute periodontitis/ acute apical abscess, 3-chronic periodontitis/ chronic apical abscess, and 4-periapical granuloma. Etiology of periapical lesions: 1-Dental caries: the reaction depends on the virulence of the micro-organism against the patient's overall defense mechanisms. -Other etiologic factors are: 2-irritating lining materials, 3-fractures of bone or teeth, 4-septicemia or pyemia (anachoretic effect), 5-gas bubbles circulating in the blood (aerodontalgia), 6-trauma of occlusion, 7-orthodontic treatment, or 8- failure of endodontic treatment. Classification 1-Early apical periodontitis (hyperemia), i.e. reversible. 2-Acute apical periodontitis and abscess (with direction taken by pus to escape from bone and their complications). 3-Chronic apical periodontitis and abscess 4-Periapical granuloma 5-Radicular cyst (will be covered with the “Cysts” topic). 1-a- Apical hyperemia:-It is the very early stage of inflammation, showing dilatation of apical vascular bed, and fluid escape, the apical periodontal tissue becomes edematous i.e. apical hyperemia. The involved tooth becomes elongated in its socket. Severe pain on slight touch that is relieved by strong pressure or occlusion on hard substances, due to pressure of exudate and chemical mediators or Dilatation of the bacterial toxins, on apical nerves. If the condition is due to dental caries, the tooth does not respond to vessels leads to fluid electrical or thermal tests. No radiographic changes escape to within the first week, only widening of the surrounding tissue, periodontal ligament (PDL) space around the apex. i.e. edema. 4 b-Acute apical periodontitis: If the condition is prolonged the tissue around the involved root is diffusely infiltrated with PMNLs, dilated vessels, RBCs as well as macrophages (acute apical periodontitis). If the irritation is not removed, bone resorption takes place. Severe pain is encountered with both slight and hard biting. Radiographically: ill-defined radiolucency, representing bone resorption. 2- Acute periapical abscess: Accumulation and localization of PMNLs at the apex of non-vital tooth, either as the initial lesion or an acute exacerbation of a chronic state, where it is termed (PHOENIX ABSCESS). Histologically:-Accumulation and localization of PMNLs leads to more intense pain that becomes increased by more pressure or percussion. The tooth still extruded until bone resorption takes place. The affected area of the jaw may be tender to palpation. Radiographically: Early changes mild thickening of the apical PDL space. In acute exacerbation of an apical granuloma or a cyst, an ill-defined radiolucency can be seen. Spread of pus from a periapical abscess & its complications: (the pus follows the line of least resistant). 1-Back to the tooth or periodontal ligament. 2-To medullary spaces (osteomyelitis). 3-Perforate the cortex (parulis or skin fistula=permanent scar). 4-To soft tissue: cellulitis and Ludwig’s angina. 5-Maxillary sinus or floor of the nose. 6-To blood vessels: bacteremia, septicemia and pyemia, (thrombophlebitis, cavernous sinus thrombosis, meningitis and intracranial abscess). 7-Trismus. 8-Lymphadenitis. 9-Pathologic fracture. 5  Gingival abscess (gum boil) Skin abscess Cellulitis Spread to the local lymph Spread to the cavernous Ludwig's angina node. sinus 3- Chronic periapical periodontitis and abscess: -The same etiologic factors with lower virulent organisms and/or enhanced immune state of the patient. -Pain is less intense, and bone resorption can be seen as an ill-defined radiolucency, in radiographs. Histologically: Diffuse infiltration of chronic inflammatory cells (periodontitis), while accumulation and localization of bacterial debri, necrotic tissue and dead chronic inflammatory cells (abscess). Granulation tissue surrounds these structures (in both apical periodontitis or abscess). 4- Periapical granuloma: -A mass of chronically inflamed granulation tissue at the apex of non-vital tooth, representing a defensive reaction secondary to spread of bacterial toxic products, or following a long standing, quiescent periapical abscess. Clinically: -Most cases are asymptomatic, become painful if acute exacerbation occurs. -The tooth may respond to pulp testing if necrosis is limited to a single root, in multi-rooted teeth. Radiographically:- a well-defined radiolucent lesion, of variable size, with radio-opaque rim, representing a long standing lesion as a way of bone defense mechanism through deposition of more calcium salts to wall-off the granulation tissue. Ill-defined radiolucency is seen in case of acute exacerbation, i.e. Phoenix abscess. 6 Histopathologic features of the apical granuloma: -Inflamed granulation tissue formed of proliferating fibroblasts and endothelial cells (new capillary formation), chronic inflammatory cells (lymphocytes, plasma cells), and macrophages. Rushton bodies (linear and arch-shape bodies). Cholesterol clefts with multinucleated giant cells. Foam cells. Epithelial rests. Russell bodies (eosinophilic globules of gamma globulin) when numerous plasma cells are present. A well-formed fibrous capsule surrounds the lesion. Osteoclasts lining the resorbed bone. Rushton bodies Osteomyelitis: is inflammation of bone and bone marrow, while osteitis means inflammation of bone only. The course and clinical presentation of the condition is affected by the site, patient's resistance and age of the person. Etiology: 1-Extension of periapical abscess. 2-A physical injury (fracture or surgery). 3- Bacteremia: Staphylococcus aureus & Streptococci are most commonly cultured from acute osteomyelitis. Any other micro-organism may be involved. 4-Non-bacterial osteomyelitis secondary to radiation therapy (i.e. osteoradionecrosis, due to reduced vascularity and destruction of osteocytes) or low grade chronic irritation as long standing periodontal disease. 5-Chronic systemic diseases, immunocompromised states, or cases of decreased vascularity, predispose patients to osteomyelitis. Classification: 1-Acute suppurative osteomyelitis (sequestrum formation) 2-Chronic suppurative osteomyelitis (moth eaten, mottled x-ray). 3-Focal sclerosing osteomyelitis (bony scar, condensing osteitis), (mosaic appearance, cotton wool). 4-Diffuse sclerosing osteomyelitis.(middle aged black females)-(involucrum). 5-Garre’s osteitis (chronic osteomyelitis with proliferative periostitis). Onion skin pattern. 6-Alveolar osteitis (dry socket). 7 I- Acute suppurative osteomyelitis: Clinically: -Fever (pyrexia), leukocytosis, lymphadenopathy, soft tissue swelling of the affected area, and drainage, with or without exfoliation of necrotic bone fragments (sequestrum). Parethesia of the lower lip, in case of mandibular involvement. -Radiographic changes do not appear usually before one Ill-defined lytic radiolucency or two weeks, as a diffuse ill-defined lytic radiolucency, (moth-eaten), and sequestrum. and individual trabeculae become fuzzy and indistinct giving a moth-eaten appearance. This is due to the acidic pH and diffuse PMNLs infiltration within marrow spaces. Histologically: Necrotic bone (sequestrum) within a purulent exudate that occupies the marrow spaces. The sequestrum shows loss of osteoblasts and osteocytes, with peripheral resorption (osteoclastic activity), and bacterial colonization. The periphery and Haversian Diffuse PMNLs, and canals contain necrotic debris and PMNLs. sequestrum. II-Chronic suppurative osteomyelitis: -It develops from unresolved acute osteomyelitis, or arise as a chronic reaction, due to long term, low grade inflammatory reaction. Clinically: Painful jaw swelling, sinus formation, purulent discharge with sequestra exfoliation. This occurs mainly in case of acute exacerbation of the chronic state?? Tooth loss or pathologic fracture, loose Mottled / moth-eaten appearance, of ill- teeth, or paresthesia is uncommon. defined radiolucency, opacities representing sequestra. Radiographically: -Mottled / moth-eaten appearance, of patchy ill-defined radiolucency, often focal opacities representing sequestra is a common finding. The cortical plate may reveal osteogenic periosteal hyperplasia. Histopathology: chronically inflamed fibrous connective tissue, filling the marrow spaces. Scattered sequestra and pockets of abscess formation are common, with lymphocytes, plasma cells and macrophages. In advanced cases, more sequestrae in necrotic marrow, dead osteocytes& osteoblasts, increased osteoclasts and inflammatory cells. In late stages, new bone starts Lymphocytes, plasma cells, and to form around sequestra (invulcrum). invulcrum. 8 III-Focal sclerosing osteomyelitis: (Condensing osteitis) or (Bony scar): Means focal bone reaction to a low grade inflammatory stimulus. An area of bone sclerosis associated with the apices of non- vital teeth with large carious lesion (usually lower premolar/molar area). Mostly in children or young adults (