Chapter 3: Pulpal and periapical disease Flashcards
Pulpitis
-‐ Chronic hyperplastic: pulp polyp (teeth with large pulp chamber-‐ molars). More in children.
Secondary/tertiary dentin
-‐ Primary dentin: formed before completion of the crown
-‐ Secondary dentin (physiologic): Follows primary dentin. Deposited throughout life gradually
-‐ Tertiary dentin: laid down in areas of focal injury.
-‐ Secondary dentin more rapid in males and in calcification-‐related diseases (arthritis, gout, kidney stones, gall stones, atherosclerosis, HT)
-‐ Progeria: accelerated aging condition. Shows widespread deposition of secondary dentin
-‐ Calcific metamorphosis: early obstruction of pulp chamber and canal with 2ary dentin deposition, after trauma. Yellow discoloration of crown
-‐ Interface dentin (fibrodentin): initial layer of reparative dentin (atubular)
Pulpal calfications
-‐ Dead tracts: tubules from dead primary odontoblasts, filled with degenrated odontob processes
-‐ Pulpal calcifications: prevalence of 20%. Assoc w/ chronic pulpitis, age and familial tendency
-‐ Pulpal calcifications: denticles (adjacent to furcation), pulp stones (coronal portion of pulp) and diffuse linear calcifications (not seen clinically)
-‐ Prominent pulpal calcifications: dentin dysplasia Id, dentin dysplasia II, pulpal dysplasia, tumoral calcinosis, calcinosis universalis and Ehler-‐Danlos syndrome
Periapical granuloma
-‐ Phoenix abscess: secondary acute inflammatory changes within a granuloma
-‐ Russel bodies: eosinophilic globules of gamma globulin in endoplasmic reticulum of plasma cells
-‐ Rushton bodies: linear or arch-‐shaped calcifications
-‐ Pyronine bodies: basophilic particles (plasma cell product)
-‐ Cholesterol clefts: from dying inflam cells, disintegrating RBCs or degenerating cystic epithelium
Periapical cyst
-‐ Originated from epithelial rests of Malassez, crevicular epithelium or fistula track epithelium
-‐ Periapical (fibrous) scar: more common when both facial and lingual cortical plates are lost
-‐ Periapical pocket cyst: incomplete epithelial lining (apex of tooth extends into cyst lumen)
-‐ Periapical true cyst: complete epithelial lining
-‐ Periapical cyst in deciduos teeth: RL surrounding roots and filling interradicular space
-‐ Residual cyst: RL that can contain a central radiopacity (from dystrophic calcification)
-‐ Prosoplasia: forward metaplasia (eg. odont epith becoming ciliated epith)
-‐ Pulse granuloma (hyaline bodies, giant-‐cell hyaline angiopathy): eosinophilic material with collagen surrounded by lymphocytes and giant cells. Represents pools of inflammatory exudate that undergo fibrosis and dystrophic calcification
Abscess
-‐ Parulis: aka gumboil. Mass of granulation tissue at opening of a sinus tract
-‐ Conditions which favor widespread infections: diabetes, neutropenia, malignancy, immunosuppresion, corticoid use, cytotoxic drug use
-‐ Cutaneous sinus: when abscess drains through the skin
Cellulitis
-‐ Acute and edematous spread of an acute inflammatory process through the ST
-‐ Most dangerous forms: Ludwig’s angina and cavernous sinus thrombosis
-‐ Ludwig’s angina: cellulitis of the sub-‐MD region. 70% from lower molar teeth infection. Also tonsillar/pharyngeal abcess, oral laceration, fractures of the mandible or submandibular sialadenitis. More in AIDS, organ transplanted, aplastic anemia and diabetes pts. Airway obstruction major concern.
-‐ Woody tongue: elevation, enlargement and protrusion of tongue in Ludwig’s angina of the subligual space
-‐ Bull neck: enlargement and tenderness of the neck (sub-‐MD space spread of LA)
-‐ Cavernous sinus thrombosis: cellulitis of the cavernous sinus in the dura. MX infections
-‐ CT: periobital enlargement involving the eyelid and conjunctiva. Proptosis (exophtalmos), chemosis (edema conjunctiva) and ptosis (dropping eyelid) seen in 90% of cases.
Osteomyelitis
-‐ Aka suppurative osteomyelitis, bacterial osteomyelitis or secondary ostemyelitis
-‐ Caused by bacterial infections, with lytic destruction and suppuration/sequestra of bone
-‐ Most due to infection or trauma. Predisponsing factors: systemic diseases, immunodeficiency, disorders with decreased vascularity (Paget’s, COD, osteopetrosis, dysosteosclerosis), tobacco, alcohol, IV drug abuse, diabetes, exanthematous fevers, malaria, sickle cell anemia, malnutrition, malignancy, collagen vascular diseases and AIDS
-‐ Acute suppurative (< 1 mth, body can’t react)
-‐ Chronic suppurative (hard to treat-‐need IV antibiotics)
-‐ Most in MD of males; maxillary cases when assoc with NUG or NOMA
-‐ Sequestrum: necrotic bone separated from adjacent vital bone
-‐ Involucrum: necrotic bone surrounded by newly-‐formed vital bone
Diffuse sclerosing osteomyelitis
-‐ Pain, inflammation and periosteal hyperplasia, slecrosis and lucency (~ FCOD and Paget’s)
-‐ Three categories: diffuse sclerosing osteomyelitis (infection present), primary chronic osteomyelitis (similar to classic chronic osteomyelitis, but no bacteria, suppuration or sequestra) and chronic tendoperiostitis
-‐ Chronic tendoperiostitis: primary chronic osteomyelitis due to overuse of masseter or digastric.
Seen at MD angle/body (masseter overuse) or anterior MD/PM region (digastric). Parafunctional habits may be found (bruxism, clenching, nail biting)
-‐ Chronic recurrent multifocal osteomyelitis (CRMO): widespread primary chronic osteomyelitis. No skin lesions, but these may appear up to 20y later (palmoplantar pustulosis, psoriasis, acne and hidradenitis suppurativa)
-‐ SAPHO (synovitis-‐acne-‐pustulosis hyperostosis-‐osteomyelitis): bone lesions (most ant chest wall) mirror primary chronic osteomyelitis and CRMO. Auto-‐immune to dermatologic bacteria, which cross-‐reacts with bone. HLA-‐27 related?
Condensing osteitis (focal sclerosing osteomyelitis)
-‐ Localized areas of bone sclerosis assoc w/ apices of teeth with pulpitis or necrosis
-‐ In children and young adults (vs. diffuse sclerosing osteomyelitis-‐ older pts)
-‐ DDx: FCOD (has RL border) and idiopathic osteosclerosis (separated from apex)
-‐ Bone scar: residual area of condensing osteitis that remains after resolution of inflammation
Osteomyelitis with proliferative periostitis
-‐ Aka periostitis ossificans and Garre’s osteomyelitis (latter is improper).
-‐ “Onion skinning” effect: active osteoblasts on convex surface of curvey bony spicules
-‐ Causes of periosteal bone formation: most osteomyelitis and neoplasms (Ewing sarcoma, LCH, osteogenic sarcoma, hemangioma). Also: trauma, cysts, infantile cortical hyperostosis, fluorosis, avitaminosis C, hypertrophic osteoarthropathy and congenital syphilis.
-‐ Rows of vital bone that parallel each other, represent periosteal reaction to inflammation
-‐ Most unifocal in molar and PM, due to caries (also periodontal infection, fracture, buccal bifurcation cysts and non-‐odontogenic infections)
Alveolar osteitis
-‐ Aka fibrinolytic alveolitis: clot is lost secondary to transf of plasminogen to plasmin, with subsequent lysis of fibrin and release of kinins (pain mediators)
-‐ Aka dry socket: clot is lost and leaves a bare bony socket
-‐ Trauma, estrogen and bacteria can stimulate fibrinolysins -‐> increased frequency in impacted 3rd molars, poor oral hygiene, inexperienced surgeon, traumatic extraction, oral contraceptive use and presurgical infection (pericoronitis). Also inadequate irrigation, smoking and heavy spitting/sucking.
-‐ Tx: xray to r/o root tip or foreign body; irrigation; analgesics; topical antibiotics(?)
