On the causes of persistent apical periodontitis
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22 59
150 Baumann & Rossman (1956) 26 74 – 121
Mortensen et al. (1970) 41 59 – 396
Bhaskar (1966) 42 48 10 2308
Spatafore et al. (1990) 42 52 6 1659
Lalonde & Luebke (1968) 44 45 11 800
Seltzer et al. (1967) 51 45 4 87 Priebe et al. (1954) 55 45 – 101 Nair Persistent apical periodontitis ª 2006 International Endodontic Journal International Endodontic Journal, 39, 249–281, 2006 261
media and the ‘pearly tumour’ of the cranium (Ander- son 1996). Accumulation of cholesterol crystals occurs in apical periodontitis lesions (Shear 1963, Bhaskar 1966, Browne 1971, Trott et al. 1973, Nair et al. 1993) with clinical significance in endodontics (Nair et al. 1993, Nair 1998). In histopathological sections, Figure 7 Structure of an apical pocket cyst. (a, b) Axial sections passing peripheral to the root canal give the false impression of a cystic lumen (LU) completely enclosed in epithelium. Sequential section (c) passing through the axial plane of the root canal clearly reveals the continuity of the cystic lumen (LU) with the root canal (RC in d). The apical foramen and the cystic lumen (LU) of the section (c) are magnified in (d). Note the pouch-like lumen (LU) of the pocket cyst, with the epithelium (EP) forming a collar at the root apex. D, Dentin (a–c ·15; d ·50). From Nair (2003a). Persistent apical periodontitis Nair International Endodontic Journal, 39, 249–281, 2006 ª 2006 International Endodontic Journal 262
such deposits of cholesterol appear as narrow elongated clefts because the crystals dissolve in fat solvents used for the tissue processing and leave behind the spaces they occupied as clefts (Fig. 10). The incidence of cholesterol clefts in apical periodontitis varies from 18% to 44% of such lesions (Shear 1963, Browne 1971, Figure 8 Structure of an apical true cyst. (a) Photomicrograph of an axial section passing through the apical foramen (AF). The lower half of the lesion and the epithelium (EP in b) are magnified in (b) and (c), respectively. Note the cystic lumen (LU) with cholesterol clefts (CC) completely enclosed in epithelium (EP), with no communication to the root canal. (a, ·15; b, ·30; c, ·180). From Nair (2003a). Reprinted with permission from Elsevier ª .
ª 2006 International Endodontic Journal International Endodontic Journal, 39, 249–281, 2006 263
Figure 9 Longitudinal radiographs (a–d) of a periapically affected central maxillary incisor of a 37-year-old woman for a period of 4 years and 9 months. Note the large radiolucent asymptomatic lesion before (a), 44 months after root-filling (b), and immediately after periapical surgery (c). The periapical area shows distinct bone healing (d) after 1 year postoperatively. Histopathological examination of the surgical specimen by modern tissue processing and step-serial sectioning technique confirmed that the lesion was a true radicular cyst that also contained cholesterol clefts. Selected radiographs from Nair et al. (1993). Persistent apical periodontitis Nair International Endodontic Journal, 39, 249–281, 2006 ª 2006 International Endodontic Journal 264
Figure 10 Cholesterol crystals and cystic condition of apical periodontitis as potential causes persistent apical periodontitis. Overview of a histological section (upper inset) of an asymptomatic apical radiolucent (Fig. 9) lesion that persisted after non- surgical 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 ¼ dentine, CT ¼ connective tissue, NT ¼ necrotic tissue. Original magnifications: ·68; upper inset ·11; lower inset ·412. From Nair (1999). Printed with permission from Australian Endodontic Journal. Nair Persistent apical periodontitis ª 2006 International Endodontic Journal International Endodontic Journal, 39, 249–281, 2006 265
Trott et al. 1973). The crystals are believed to be formed from cholesterol released by: (i) disintegrating erythrocytes of stagnant blood vessels within the lesion (Browne 1971), (ii) lymphocytes, plasma cells and macrophages which
die in great numbers and
disintegrate in chronic periapical lesions, and (iii) the circulating plasma lipids (Shear 1963). All these sources may contribute to the concentration and crystallization of cholesterol in periapical area. Never- theless, locally dying inflammatory cells may be the major source of cholesterol as a result of its release from disintegrating membranes of such cells in long-stand- ing lesions (Seltzer 1988, Nair et al. 1993). Cholesterol crystals are intensely sclerogenic (Abdul- la et al. 1967, Bayliss 1976). They induce granuloma- tous lesions in dogs (Christianson 1939), mice (Spain et al. 1959, Adams et al. 1963, Abdulla et al. 1967, Adams & Morgan 1967, Bayliss 1976) and rabbits (Hirsch 1938, Spain et al. 1959, Spain & Aristizabal 1962). In an experimental study that specifically investigated the potential association of cholesterol crystals and non-resolving apical periodontitis lesions (Nair et al. 1998), pure cholesterol crystals were placed in Teflon cages that were implanted subcutaneous in guinea-pigs. The cage contents were retrieved after 2, 4 and 32 weeks of implantation and processed for light and electron microscopy. The cages revealed (Fig. 11) delicate soft connective tissue that grew in through perforations on the cage wall. The crystals were densely surrounded by numerous macrophages and multinu- cleate giant cells forming a well circumscribed area of tissue reaction. The cells, however, were unable to eliminate the crystals during an observation period of 8 months. The accumulation of macrophages and giant cells around cholesterol crystals suggests that the crystals induced a typical foreign-body reaction (Coleman et al. 1974, Nair et al. 1990b, Sjo¨gren et al. 1995). The macrophages and giant cells that surround cholesterol crystals are not only unable to degrade the crystalline cholesterol but are major sources of apical inflammatory and bone resorptive mediators. Bone resorbing activity of cholesterol-exposed macrophages due to enhanced expression of IL-1 a has been experi- mentally shown (Sjo¨gren et al. 2002). Accumulation of cholesterol crystals in apical periodontitis lesions (Fig. 10) can adversely affect post-treatment healing of the periapical tissues as has been shown in a long- term longitudinal follow-up of a case in which it was concluded that ‘the presence of vast numbers of cholesterol crystals … would be sufficient to sustain the lesion indefinitely’ (Nair et al. 1993). The evidence from the general literature reviewed (Nair 1999) is clearly in support of that assumption. Therefore, accumulation of cholesterol crystals in apical perio- dontitis lesions can prevent healing of periapical tissues after non-surgical root canal treatment, as such retreatment cannot remove the tissue irritating choles- terol crystals that exist outside the root canal system. Foreign bodies Foreign materials trapped in periapical tissue during and after endodontic treatment (Nair et al. 1990b, Koppang et al. 1992) can perpetuate apical periodon- titis persisting after root canal treatment. Materials used in non-surgical root canal treatment (Nair et al. 1990b, Koppang et al. 1992) and certain food particles (Simon et al. 1982) can reach the periapex, induce a foreign body reaction that appears radiolucent and remain asymptomatic for several years (Nair et al. 1990b). Gutta-percha The most frequently used root canal filling material is gutta-percha in the form of cones. The widely held view that it is biocompatible and well tolerated by human tissues is inconsistent with the clinical observation that extruded gutta-percha is associated with delayed heal- ing of the periapex (Strindberg 1956, Seltzer et al. 1963, Kerekes & Tronstad 1979, Nair et al. 1990b, Sjo¨gren et al. 1990). Large pieces of gutta-percha are well encapsulated in collagenous capsules (Fig. 12), but fine particles of gutta-percha induce an intense, localized tissue response (Fig. 13), characterized by the presence of macrophages and giant cells (Sjo¨gren et al. 1995). The congregation of macrophages around the fine particles of gutta-percha is important for the clinically observed impairment in the healing of apical periodon- titis when teeth are root filled with excess material. Gutta-percha cones contaminated with tissue irritating materials can induce a foreign body reaction at the periapex. In an investigation on nine asymptomatic apical periodontitis lesions that were removed as surgical block biopsies and analysed by correlative light and electron microscopy, one biopsy revealed the involvement of contaminated gutta-percha (Nair et al. 1990b). The radiolucency grew in size but remained asymptomatic for a decade of post-treatment follow-up (Fig. 14). The lesion was characterized by the presence of vast numbers of multinucleate giant cells with Persistent apical periodontitis Nair International Endodontic Journal, 39, 249–281, 2006 ª 2006 International Endodontic Journal 266
Figure 11 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 that rhomboid clefts left by cholesterol crystals (CC) surrounded by giant cells (GC) and numerous mononuclear cells (arrowheads in d). AT ¼ adipose tissue, CT ¼ connective tissue. Original magnifications: (a) ·10, (b) ·21, (c) ·82 and (d) ·220. From Nair (1999). Printed with permission from Australian Endodontic Journal. Nair Persistent apical periodontitis ª 2006 International Endodontic Journal International Endodontic Journal, 39, 249–281, 2006 267
birefringent inclusion bodies (Fig. 15). In transmission electron microscope the birefringent bodies were highly electron dense (Fig. 16). An X-ray microanalysis of the inclusion bodies using scanning transmission electron microscope (STEM) revealed the presence of magnesium and silicon (Fig. 17). These elements are presumably the remnants of a talc-contaminated gutta-percha that protruded into the periapex and had been resorbed during the follow-up period. Other plant materials Vegetable food particles, particularly leguminous seeds (pulses), and materials of plant origin that are used in endodontics can get lodged in the periapical tissue before and/or during the treatment procedures and prevent healing of the lesion. Oral pulse granuloma is a distinct histopathological entity (King 1978). The lesions are also referred to as the giant cell hyaline angiopathy (Dunlap & Barker 1977, King 1978), vegetable granuloma (Harrison & Martin 1986) and food-induced granuloma (Brown & Theaker 1987). Pulse granuloma has been reported in lungs (Head 1956), stomach walls and peritoneal cavities (Sherman & Moran 1954). Experimental lesions have been induced in animals by intratracheal, intraperitonial and submucous introduction of leguminous seeds (Knoblich 1969, Talacko & Radden 1988b). Periapical pulse granuloma are associated with teeth damaged by caries and with the antecedence of endodontic treat- ment (Simon et al. 1982, Talacko & Radden 1988a). Pulse granuloma are characterized by the presence of intensely iodine and PAS positive hyaline rings or bodies surrounded by giant cells and inflammatory cells (Mincer et al. 1979, Simon et al. 1982, Talacko & Radden 1988a,b). Leguminous seeds are the most frequently involved vegetable food material in such granulomatous lesions. This indicates that certain components in pulses such as antigenic proteins and mitogenic phytohaemagglutinins may be involved in the pathological tissue response (Knoblich 1969). The pulse granuloma are clinically significant because particles of vegetable food materials can reach the periapical tissue via root canals of teeth exposed to the oral cavity by trauma, carious damage or by endodon- tic procedures (Simon et al. 1982). Apical periodontitis developing against particles of predominantly cellulose-containing materials that are used in endodontic practice (White 1968, Koppang et al. 1987, 1989, Sedgley & Messer 1993) has been denoted as cellulose granuloma. The cellulose in plant materials is a granuloma-inducing agent (Knoblich Figure 12 Guinea-pig tissue reaction to gutta-percha (GP) by 1 month after subcutaneous implantation (a). Large pieces of gutta- percha are well encapsulated by collagen fibres that run parallel to the surface of the gutta-percha particle. The interface of the gutta-percha particle and the host tissue (arrow) is magnified in stages in (b) and (c). The gap between the implant and the collagen capsule is artefactual. Note the non-inflamed, healthy soft delicate connective tissue. Original magnifications: (a) ·42, (b)
·80, (c) ·200. From Nair (2003b). Persistent apical periodontitis Nair International Endodontic Journal, 39, 249–281, 2006 ª 2006 International Endodontic Journal 268
Figure 13 Disintegrated gutta-percha as potential cause of persistent apical periodontitis. As clusters of fine particles (a) they induce intense circumscribed tissue reaction (TR) around. Note that the fine particles of gutta-percha (*in c, GP in d) are surrounded by numerous mononuclear cells (MNC). Original magnifications: (a) ·20, (b) ·80, (c) ·200, (d) ·750. From Nair (2003b).
Nair Persistent apical periodontitis ª 2006 International Endodontic Journal International Endodontic Journal, 39, 249–281, 2006 269
1969). Endodontic paper points (Fig. 18) are utilized for microbial sampling and drying of root canals. Sterile and medicated cotton wool has been used as an apical seal. Particles of these materials can dislodge or get pushed into the periapical tissue (White 1968) so as to induce a foreign body reaction at the periapex. The resultant clinical situation may be a ‘prolonged, extremely troublesome and disconcerted course of events’ (White 1968). Presence of cellulose fibres in periapical biopsies with a history of previous endodon- tic treatment has been reported (Koppang et al. 1987, 1989, Sedgley & Messer 1993). The endodontic paper points and cotton wool consists of cellulose that cannot be degraded by human body cells. They remain in tissues for long periods of time (Sedgley & Messer 1993) and induce a foreign body reaction around them. The particles, in polarized light, are birefringent due to the regular structural arrangement of the molecules within cellulose (Koppang et al. 1989). Infected paper points can protrude through the apical foramen (Fig. 18) and allow a biofilm to grow around it. This will sustain and even intensify the apical periodontitis after root canal treatment eventually leading to a failure of treatment. Other foreign materials They include amalgam, endodontic sealants and cal- cium salts derived from periapically extruded Ca(OH) 2 .
of 29 apical biopsies 31% of the specimens were found to contain materials compatible with amalgam and endo- dontic sealer components (Koppang et al. 1992). Scar tissue healing There is evidence (Penick 1961, Bhaskar 1966, Seltzer et al. 1967, Nair et al. 1999) that unresolved periapical radiolucencies may occasionally be due to healing of Figure 14 Two longitudinal radiographs (inset and a) of a root filled and periapically affected left central maxillary incisor of a 54-year-old man. The first radiograph (inset) taken immediately after root filling in 1977 shows a small excess filling that protrudes into the periapex (arrowhead in inset). Note the excess filling has disappeared in the radiograph taken 10 years later (arrowhead in a) and shortly before surgery was performed. The apical block-biopsy removed by surgery does not show any excess filling as is evident from the macrophotograph of the decalcified and axially subdivided piece of the biopsy (b). RF, root filling, D, dentine, GR, granuloma. Original magnification (b) ·10. From Nair et al. (1990b). Printed with permission from Lippincott Williams & Wilkins ª .
International Endodontic Journal, 39, 249–281, 2006 ª 2006 International Endodontic Journal 270
Figure 15 Talc-contaminated gutta-percha as a potential cause of non-healing apical periodontitis. 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 lights (b). Note the birefringent bodies distributed throughout the lesion (b). The apical foramen is magnified in (c) and the dark arrow-headed 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, dentine. Magnifications: (a, b) ·25; (c) ·66; (d) ·370. From P.N.R. Nair, Pathology of apical periodontitis. In: Ørstavik D, Pitt Ford TR, eds. Essential Endodontology. Oxford, 1998. Nair Persistent apical periodontitis ª 2006 International Endodontic Journal International Endodontic Journal, 39, 249–281, 2006 271
the lesion by scar tissue (Fig. 19) that may be misdi- agnosed as a radiographic sign of failed endodontic treatment. Little is known about the tissue dynamics of periapical healing after non-surgical root canal treat- ment and periapical surgery. However, certain deduc- tions can be made from the data available on normal healing and guided regeneration of the marginal periodontium. Various tissue cells participate in the healing process. The pattern of healing depends on several factors, two of which are decisive. They are the regeneration potential and the speed with which the tissue cells bordering the defect react (Karring et al. 1980, 1993, Nyman et al. 1982, Schroeder 1986). A periapical scar probably develops because precursors of soft connective tissue colonize both the root tip and periapical tissue; this may occur before the appropriate cells, which have the potential to restore various structural components of the apical periodontium are able to do so (Nair et al. 1999). Conclusions This review of the literature leads to the conclusion that there are six biological factors that contribute to the Figure 16 Low magnification transmission electron micrograph showing the profiles of several giant cells within the apical periodontitis shown in Figs. 14 & 15. Note the presence of many slit-like inclusion bodies (BB 1 to BB 6 ), which contain a highly electron-dense material. This material may remain intact within the inclusion body, may be pushed away from its original site (BB
2 ) or may appear disintegrated (BB 3 and BB
4 ) by the tissue processing. Note the lines of artefacts AL, which are created by portions of the electron dense material having been carried away by the knife-edge, leaving tracts behind. Original magnification ·1880. From Nair et al. (1990b). Printed with permission from Lippincott Williams & Wilkins ª .
International Endodontic Journal, 39, 249–281, 2006 ª 2006 International Endodontic Journal 272
Figure 17 High magnification transmission electron micrograph (c) of the intact birefringent body labelled BB1 in Fig. 3. Note the distinct delimiting membrane around the birefringent body (BB). Energy-dispersive X-ray microanalysis of the electron dense material done in scanning-transmission electron microscope (STEM: done at the point where the two hairlines perpendicular to each other cross in the left inset) revealed the presence of silicon (Si), magnesium (Mg) and lead (Pb) in (a) whereas another site in the neighbouring cytoplasm of the same giant cell (right inset) does not show the presence of Si and Mg (b). Lead and uranium (U) are used for section contrasting and emission in copper (Cu) is from the section-supporting grid made of copper. Original magnification ·11 000; insets ·3300. From Nair et al. (1990b). Printed with permission from Lippincott Williams & Wilkins ª . Nair Persistent apical periodontitis ª 2006 International Endodontic Journal International Endodontic Journal, 39, 249–281, 2006 273
Figure 18 A massive paper-point granuloma affecting a root-canal-treated human tooth (a). The demarcated area in (b) is Yüklə 337,83 Kb. Dostları ilə paylaş:
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