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PATHOGENESIS OF APICAL PERIODONTITIS AND THE CAUSES OF ENDODONTIC FAILURES

Institute of Oral Biology, Section of Oral Structures and Development, Center of Dental and Oral Medicine, University of Zürich, Plattenstrasse 11, CH-8028 Zürich, Switzerland; nair{at}zzmk.unizh.ch

View larger version (191K): [in a new window]   Figure 1. Endodontic microflora of a human tooth with apical periodontitis (GR). The areas between the upper two and the lower two arrowheads in (a) are magnified in (b) and (c), respectively. Note the dense bacterial aggregates (BA) sticking (b) to the dentinal (D) wall and also remaining suspended among neutrophilic granulocytes in the fluid phase of the root canal (c). A transmission electron microscopic view (d) of the pulpo-dentinal interface shows bacterial condensation on the surface of the dentinal wall, forming thick, layered biofilm. Magnifications: (a) 46x; (b) 600x; (c) 370x; and (d) 2350x. (From Nair, 1997.)

View larger version (165K): [in a new window]   Figure 2. Well-entrenched biofilm at the apical foramen of a tooth affected with apical periodontitis (GR). The apical delta in (a) is magnified in (b). The canal ramifications on the left and right in (b) are magnified in (c) and (d), respectively. Note the strategic location of the bacterial clusters (BA) at the apical foramina. The bacterial mass appears to be held back by a wall of neutrophilic granulocytes (NG). Obviously, any surgical and/or microbial sampling procedures of the periapical tissue would contaminate the sample with the intraradicular flora. EP, epithelium. Magnifications: (a) 20x, (b) 65x, and (c,d) 350x. (From Nair, 2002.)

View larger version (179K): [in a new window]   Figure 3. The primary body cells involved in the pathogenesis of apical periodontitis. Neutrophils (NG in a) in combat with bacteria (BA) in an exacerbating apical periodontitis. Lymphocytes (LY in b) are the major components of chronic apical periodontitis, but their subpopulations cannot be identified on a structural basis. Plasma cells (PL in c) form a significant component of chronic asymptomatic lesions. Note the highly developed rough endoplasmic reticulum of the cytoplasm and the localized condensation of heterochromatin subjacent to the nuclear membrane, which gives the typical ‘cartwheel’ appearance in light microscopy. Macrophages (MA in d) are voluminous cells with elongated or U-forming nuclei and cytoplasm with rough endoplasmic reticulum. Magnifications: (a,b,c,d) 3900x. (From Nair, 1998b.)

View larger version (22K): [in a new window]   Figure 4. Pathogenesis of acute (a,b), chronic (c), and cystic (d,e) apical periodontitis (AP) lesions. The acute lesion may be primary (a) or secondary (b) and is characterized by the presence of a focus of neutrophils (PMNs). The major components of chronic lesions (c) are lymphocytes (Ly), plasma cells (Pc), and macrophages (Ma). Periapical cysts can be differentiated into true cysts (d), with completely enclosed lumina, and pocket cysts (e), with cavities open to the root canal. Arrows indicate the direction in which the lesions can change. (From Nair, 1998b.)

View larger version (171K): [in a new window]   Figure 5. A microbial biofilm at the root-tip of a human tooth with secondary acute apical periodontitis of endodontic origin. The mixed bacterial flora consists of numerous dividing cocci, rods (lower inset), filaments (FI), and spirochetes (S, upper inset). Rods often reveal a Gram-negative cell wall (GW, lower inset). C, cementum; D, dentin. Magnifications: 2680x; upper inset x 19,200; lower inset x 36,400. (Adapted from Nair, 1987.)

View larger version (168K): [in a new window]   Figure 6. Structure of apical true cysts (a,b). The cyst lumina (LU) are completely enclosed in stratified squamous epithelium (EP). Note the absence of any communication of the cyst lumen with the root canal (RC in b). The demarcated area in a is magnified in c. Arrowheads in c indicate cholesterol clefts. Magnifications; (a) 30x, (b) 17x, and (c) 60x. (From Nair et al., 1996.)

View larger version (150K): [in a new window]   Figure 7. Structure of an apical pocket cyst. Axial sections passing peripheral to the root canal (a,b) give the false impression of the presence of a cyst lumen (LU) completely enclosed in epithelium. Sequential section (c,d) passing through the axial plane of the root canal (RC) clearly reveals the continuity of the cystic lumen (LU) with the root canal (RC). Note the pouch-like lumen (LU) of the pocket cyst with the epithelium (EP), forming a collar at the root apex. Magnifications: (a,b,c) 5x; (d) 132x. (Adapted from Nair, 1995.)

View larger version (163K): [in a new window]   Figure 8. Axial sections through the surgically removed apical portion of the root with a therapy-resistant apical periodontitis. Note the light microscopically visible cluster of bacteria (BA in a) in the root canal. Serial semi-thin sections (b to e), taken at various distances from the section plane of (a), reveal the emerging and gradually widening profiles of an accessory root canal (AC) that is clogged with bacteria (BA). Magnifications: (a) 52x, (b-e) 62x. (From Nair et al., 1990a.)

View larger version (201K): [in a new window]   Figure 9. Transmission electron microscopic view of the bacterial mass (BA, upper inset) illustrated in (8a). Morphologically, the bacterial population appears to be composed of only Gram-positive, filamentous organisms (arrowhead in lower inset). Note the distinctive Gram-positive cell wall. The upper inset is a magnification of the bacterial cluster (BA) in (8a). Magnification: 3400x. Insets: upper, 132x; lower, 21,300x. (From Nair et al., 1990a.)

View larger version (162K): [in a new window]   Figure 10. Fungi as a potential cause of endodontic failures. (a) Low-power overview of an axial section of a root-filled (RF) tooth with a persisting apical periodontitis lesion (GR). The rectangular demarcated areas in (a) and (d) are magnified in (d) and (b), respectively. Note the two microbial clusters (arrowheads in b) further magnified in (c). The oval inset in (d) is a transmission electron microscopic view of the organisms. Note the electron-lucent cell wall (CW), nuclei (N), and budding forms (BU). Magnifications: (a) 35x, (b) 130x, (c) 330x, (d) 60x, and oval inset, 3400x. (Adapted from Nair et al., 1990b.)

View larger version (138K): [in a new window]   Figure 11. An Actinomyces-infected periapical pocket cyst affecting a human maxillary first premolar (radiographic inset). The cyst is lined with ciliated columnar (CEP) and stratified squamous (SEP) epithelia. The rectangular block in (a) is magnified in (c). The typical ‘ray-fungus’ type of actinomycotic colony (AC in b) is a magnification of the one demarcated in (c). Note the two black-arrowheaded, distinct actinomycotic colonies (AC in c) within the lumen (LU). Magnifications: (a) 20x, (b) 60x, and (c) 210x. (From Nair et al., 2002.)

View larger version (177K): [in a new window]   Figure 12. Cholesterol crystals and cystic condition of apical periodontitis as potential causes for endodontic failures. Overview of a histological section (upper inset) of an asymptomatic apical periodontitis that persisted after conventional root canal treatment. Note the vast number of cholesterol clefts (CC) surrounded by giant cells (GC), of which a selected one with several nuclei (arrowheads) is magnified in the lower inset. D = dentin, CT = connective tissue, NT = necrotic tissue. Magnifications: x68. Upper inset, 11s; lower inset, 412s. (From Nair, 1999.)

View larger version (135K): [in a new window]   Figure 13. Photomicrograph (a) of guinea pig tissue reaction to aggregates of cholesterol crystals after an observation period of 32 weeks. The rectangular demarcated areas in (a), (b), and (c) are magnified in (b), (c), and (d), respectively. Note the rhomboid clefts left by cholesterol crystals (CC) surrounded by giant cells (GC) and numerous mononuclear cells (arrowheads in d). AT = adipose tissue, CT = connective tissue. Magnifications: (a) 10x, (b) 21x, (c) 82x, and (d) 220x. (From Nair, 1999.)

View larger version (138K): [in a new window]   Figure 14. Disintegrated gutta-percha as potential cause of endodontic failures. As clusters of fine particles (a), they induce intense circumscribed tissue reaction (TR) around the particles. The regular demarcated area in (a) is magnified in (b). Note that the fine particles of gutta-percha (* in c, GP in d) are surrounded by numerous mononuclear cells (MNC). Magnifications: (a) 30x, (b) 80x, (c) 200x, and (d) 750x. (From Nair, 2002.)

View larger version (127K): [in a new window]   Figure 15. Talc-contaminated gutta percha as a potential cause of endodontic failure. Note the apical periodontitis (AP) characterized by foreign-body giant cell reaction to gutta-percha cones contaminated with talc (a). The same field when viewed in polarized light (b). Note the birefringent bodies distributed throughout the lesion (b). The apical foramen is magnified in (c), and the dark-arrowheaded cells in (c) are further enlarged in (d). Note the birefringence (BB) emerging from slit-like inclusion bodies in multinucleated (N) giant cells. B, bone; D, dentin. Magnifications: (a,b) 25x; (c) 66x; and (d) 300x. (From Nair, 1998b.)

View larger version (153K): [in a new window]   Figure 16. A massive paper-point granuloma affecting a root-canal-treated human tooth (a). The demarcated area in (b) is magnified in (c) and further magnified in (d). Note the tip of the paper point (FB) projecting into the apical periodontitis lesion and the bacterial plaque (BP) adhering to the surface of the paper point. RT, root tip; EP, epithelium; PC, plant cell. Magnifications: (a) 20x, (b) 40x, (c) 60x, and (d) 150x. (From Nair, 2002.)