Histopathology
Changes occurring in the initial stages of gingival inflammation are presented in Chapter 16. Once the pocket is formed, several microscopic features are present, as discussed in the following sections.
Soft Tissue Wall
The connective tissue is edematous and densely irtfiltrated with plasma cells (approximately 80%),86 lymphocytes, and a scattering of PMNs. The blood vessels are increased in number, dilated, and engorged, particularly in the subepithelial connective tisstie layer.11 The connective tissue exhibits varying degrees of degeneration. Single or multiple necrotic foci are occasionally present/" In addition to exudative and degenerative changes, the connective tissue shows proliferation of the endothelial cells, with newly formed capillaries, fibroblasts, and collagen fibers (Fig. 22-5).
The junctional epithelium at the base of the pocket is usually much shorter than that of a normal sulcus. Although marked variations are found as to length, width, and condition of the epithelial cells, usually the coronoapical length of the junctional epithelium is reduced to only 50 to 100 ¿un.,s The cells may be well formed and in good condition or may exhibit slight to marked degeneration (Fig. 22-6).
The most severe degenerative changes in the periodontal pocket occur along the lateral wall (Fig. 22-7). The epithelium of the lateral wall of the pocket presents striking proliferative and degenerative changes. I pithelial buds or interlacing cords of epithelial cells project from the lateral wall into the adjacent inflamed connective tissue and may extend farther apically than the junctional epithelium. These epithelial projections, as well as the remainder of the lateral epithelium, are densely infiltrated by leukocytes and edema from the inflamed connective tissue. The cells undergo vacuolar degeneration and rupture to form vesicles. Progressive degeneration and necrosis of the epithelium lead to ulceration of the lateral wall, exposure of the underlying inflamed connective tissue, and suppuration. In some cases, acute inflammation is superimposed on the underlying chronic changes.
A comparative study of gingival histopathologic changes in rapidly progressive (aggressive) and adult periodontitis (chronic)w revealed more pronounced degenerative changes in the epithelium of aggressive cases with more open intercellular spaces, with micro-clefts and necrotic areas.
The severity of the degenerative changes is not necessarily related to pocket depth. Ulceration of the lateral wall may occur in shallow pockets, and deep pockets are occasionally observed in which the lateral epithelium is relatively intact or shows only slight degeneration.
The epithelium at the gingival crest of a periodontal pocket is generally intact and thickened, with prominent rete pegs.
A detailed electron microscopic study of the pocket epithelium in experimentally induced pockets in dogs has been performed b\ MtillcMilauserand Schroder."1
Bacterial Invasion. Bacterial invasion ol the apical and lateral areas of the pocket wall has been desc ribed in
Fig. 22-5 Left, Interdental papilla with suprabony pockets on proximal tooth surfaces. D, Densely inflamed connective tissue; E, proliferating pocket epithelium, U, ulcerated pocket epithelium. Right, Magnification of the rectangular area on the left. Note the ulcerated area (U) and the infiltrate between the collagen fibers.
Fig. 22-5 Left, Interdental papilla with suprabony pockets on proximal tooth surfaces. D, Densely inflamed connective tissue; E, proliferating pocket epithelium, U, ulcerated pocket epithelium. Right, Magnification of the rectangular area on the left. Note the ulcerated area (U) and the infiltrate between the collagen fibers.
Fig. 22-6 A, Low-power section of periodontal pocket (P). the location of the junctional epithelium is indicated by the arrow (FA). The lateral epithelial wall is ulcerated B, Detailed study of junctional epithelium (LA) at the base of the pocket (P) Note the extension of well-formed epithelial cells (arrow) along the re-sorbed root surface. There is a dense accumulation of leukocytes enclosed within the epithelium.
Fig. 22-6 A, Low-power section of periodontal pocket (P). the location of the junctional epithelium is indicated by the arrow (FA). The lateral epithelial wall is ulcerated B, Detailed study of junctional epithelium (LA) at the base of the pocket (P) Note the extension of well-formed epithelial cells (arrow) along the re-sorbed root surface. There is a dense accumulation of leukocytes enclosed within the epithelium.
Fig. 22-7 A, Low-power view of the lateral wall ot a periodontal pocket. Note the dense inflammatory infiltrate and the proliferating epithelium B, Hi<jh-power view of the rectangular area in A. Note the areas of atrophic epithelium (o) and epithelial proliferation (p) The connective tissue is densely infiltrated (i); some remnants of collagen libers (c) can fie seen.
Fig. 22-7 A, Low-power view of the lateral wall ot a periodontal pocket. Note the dense inflammatory infiltrate and the proliferating epithelium B, Hi<jh-power view of the rectangular area in A. Note the areas of atrophic epithelium (o) and epithelial proliferation (p) The connective tissue is densely infiltrated (i); some remnants of collagen libers (c) can fie seen.
human chronic periodontitis, l ilainents, rods, and coc-coid organisms with predominant gram-negative cell walls have been found in intercellular spaces of the epithelium.27 >s Hillmann et alw have reported Ihe presence of Porphyroiwnns gingivnli\ and hcvoleiUi hitcrnicihn in the gingiva of aggressive periodontitis cases. Acthwbncil-¡USQctinoinycetenicoinitans has also been found in the ns-
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Bacteria may invade the intercellular space under exfoliating epithelial cells, but they are also found between deeper epithelial cells and accumulating on the basement lamina. Some bacteria traverse the basement lamina and invade the subepithelial connective tissue"1 (Figs. 22-H and 22-9).
The presence ol bacteria in the gingival tissues has been interpreted by different investigators as bacterial invasion or as passive translocation of plaque bacteria. I bis important point has significant clinicopathologic implications and has not yet been clarified.18 H r
Microtopography of the Gingival Wall of the Pocket
Scanning electron microscopy has permitted the description of several areas in the soft tissue wall ol the )ocket where different types of activity take place.00These areas are irregularly oval or elongated and adjacent to one another and measure about 50 to 200 ¿¿in. these findings suggest that the pocket wall is constantly changing as a
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Ficj. 22-8 Electron micrograph of a section of pocket wall in advanced periodontitis in a human specimen, showing bacterial penetration into the epithelium and connective tissue. Scanning electron microscope view of surface ol pocket wall (A), sectioned epithelium (R), and sectioned connective tissue (C) Curved arrows point to areas of bacterial penetration into ihe epithelium. Thick white arrows point to bacterial penetration into the connective tissue through a break in the continuity of the basal lamina. CI, Connective tissue fibers; D, accumulation ol bacteria (rods, cocci, filaments) on basal lamina; f. lilamentous organism on surface ol epithelium. Asterisk points to coccobacillus in connective tissue.
Ficj. 22-8 Electron micrograph of a section of pocket wall in advanced periodontitis in a human specimen, showing bacterial penetration into the epithelium and connective tissue. Scanning electron microscope view of surface ol pocket wall (A), sectioned epithelium (R), and sectioned connective tissue (C) Curved arrows point to areas of bacterial penetration into ihe epithelium. Thick white arrows point to bacterial penetration into the connective tissue through a break in the continuity of the basal lamina. CI, Connective tissue fibers; D, accumulation ol bacteria (rods, cocci, filaments) on basal lamina; f. lilamentous organism on surface ol epithelium. Asterisk points to coccobacillus in connective tissue.
- f-ig. 22 9 Transmission electron micrograph of the epithelium in the periodontal pocket wall showing bacteria in the intercellular spaces, ft Bacteria; LC, epithelial cell; IS, intercellular space; L, leukocyte about to enyull bacteria. Magnification ■ 8000.
Fig. 22-11 Scanning electron micrograph ol the periodontal pocket wall, frontal view, in a case of advanced periodontitis in a human. Note the desquamating epithelial cells and leukocytes (while arrows) emerging onto the pocket space. Scattered bacteria can also be seen (black arrow). Magnification 1500
Fig. 22-11 Scanning electron micrograph ol the periodontal pocket wall, frontal view, in a case of advanced periodontitis in a human. Note the desquamating epithelial cells and leukocytes (while arrows) emerging onto the pocket space. Scattered bacteria can also be seen (black arrow). Magnification 1500
Fig. 22 10 Scanning electron frontal micrograph ol the periodontal pocket wall. Different areas can be seen in the pocket wall surface A, Area ol quiescence; B, bacterial accumulation; C, bacterial-leukocyte interaction; D, intense cellular desquamation Arrows point to emerging leukocytes and holes left by them in the pocket wall. Magnilication 800.
Fig. 22 10 Scanning electron frontal micrograph ol the periodontal pocket wall. Different areas can be seen in the pocket wall surface A, Area ol quiescence; B, bacterial accumulation; C, bacterial-leukocyte interaction; D, intense cellular desquamation Arrows point to emerging leukocytes and holes left by them in the pocket wall. Magnilication 800.
result of the interaction between the host and the bacteria. I he following areas have been noted:
1. Areas of relative ifiiiescence, showing a relatively flat surface with minor depressions and mounds and occasional shedding of cells (Fig. 22-10, .4).
2. Areas of bacterial accumulation, which appear as depressions on the epithelial surface, with abundant debris and bacterial clumps penetrating into the enlarged intercellular spaces. These bacteria are mainly cocci, rods, and Filaments, with a few spirochetes (see Fig. 22-10, /*).
3. Areas of emergence of leukocytes, where leukocytes appear in the pocket wall through holes located in the intercellular spaces (Fig. 22-11 >.
4. Areas of leukocyte-bacteria interaction, where numerous leukocytes are present and covered with bacteria in an apparent process of phagocytosis. Bacterial plaque associated with the epithelium is seen either as an organized matrix covered by a librin-like material in contact with the surface of cells or as bacteria penetrating into the intercellular spaces (see I ig. 22-10, < ).
5. Areas of intense epithelial desquamation, which consist of semi-attached and folded epithelial squamcs, sometimes partially covered with bacteria (Fig. 22-10, D).
6. Areas of ulceration, with exposed connective tissue (Fig. 22-12).
7. Areas of hemorrhage, with numerous erythrocytes.
Fhe transition from one area to another could be postulated as follows: bacteria accumulate in previously quiescent areas, triggering the emergence ol leukocytes and
I'he Periodontal Pocket " ( HAITI K 22 343
Fig. 22-12 left, Area ol ulceration in the lateral wall ol a deep periodontal pocket in a human specimen. A, Surface of pocket epithelium in a quiescent state; B, area ol hemorrhage. Magnification - 800. Right, Magni-lication ol the square area on the left Connective tissue fibers and cells can be seen in the bottom of the ulcer. Scanning electron microscopy. Magnification 4000.
Fig. 22-12 left, Area ol ulceration in the lateral wall ol a deep periodontal pocket in a human specimen. A, Surface of pocket epithelium in a quiescent state; B, area ol hemorrhage. Magnification - 800. Right, Magni-lication ol the square area on the left Connective tissue fibers and cells can be seen in the bottom of the ulcer. Scanning electron microscopy. Magnification 4000.
Fig. 22-13 Periodontal pocket wall. The inner half is inflamed and ulcerated; the outer half is densely collagenous.
the leukocyte-bacteria interaction. I bis would lead to intense epithelial desquamation and finally to ulceration and hemorrhage.
Periodontal Pockets as Healing Lesions
Periodontal pockets «ire chronic inflammatory lesions and as such are constantly undergoing repair. < omplete healing does not occur because of the persistence of the bacterial attack, which continues to stimulate an inflammatory response, causing degeneration ol the new tissue elements formed in the continuous effort at repair.
The condition of the soft tissue wall of the periodontal pocket results from the interplay of the destructive and constructive tissue changes. Iheir balance determines clinical features such as color, consistency, and surface texture of the pocket wall. II the inflammatory fluid and cellular exudate predominate, the pocket wall is bluish-red, soft, spongy, and friable, with a smooth, shiny surface. If there is a relative predominance of newly formed connective tissue cells and fibers, the pocket wall is more firm and pink. At the clinical level, the former condition is generally referred in as an edematous pocket wall and the latter as a fibrotic pocket wall (see (Ihapter 30).
Edematous and fibrotic pockets represent opposite extremes of the same pathologic process, not different disease entities. Thee are subject to constant modification, depending on the relative predominance of exudative and constructive changes.
fibrotic pocket watts may be misleuding because the) tlo not necessarily reflect what is hiking place throughout the pocket wall, The most severe degenerative changes in
Fig. 22-13 Periodontal pocket wall. The inner half is inflamed and ulcerated; the outer half is densely collagenous.
periodontal tissues occur adjacent to I lie tooth surface and subgingival plaque. In some cases, inflammation and ulceration on the inside ol the pocket are walled oil by fibrous tissue on the outer aspect (fig. 22-13). Outwardly the pocket appears pink and fibrotic. despite the inflammatory changes occ urring within.
- Fig. 22-14 Interdental papilla (I) with ulcerated suprabony periodontal pockets on its mesial and distal aspects. Calculus is present on the approximal tooth surfaces and within the gingiva (arrow). The hone is shown at H
Pocket Contents
Periodontal pockets contain debris consisting principally of microorganisms and their products (enzymes, endotoxins, and other metabolic products), gingival lluid, food remnants, salivary mucin, desquamated epithelial cells, and leukocytes. Plaque-covered calculus usually projects from the tooth surface (1 ig. 22-14). Purulent exudate, il present, consists of living, degenerated, and necrotic leukocytes; living and dead bacteria; serum; and a scant amount of fibrin.so I he contents of periodontal pockets filtered free of organisms and debris have been demonstrated to be toxic when injected subcutancously into experimental animals.
Significance of Pus formation. I'here is a tendency to overemphasize the importance of the purulent exudate and to equate it with severity of periodontal disease. Because it is a dramatic clinical finding, early observers assumed thai it was responsible lor the loosening and exfoliation of the teeth. Pus is a common feature of periodontal disease, but it is only a secondaiy sign, l ire presence ol ptts or the ease with which it can be expressed from the pocket merely reflects the nature of the inflammatory changes in the pocket wall. It is not an indication of the depth of the pocket or the severity Of the destruction ot the supporting tissues. Kxtensive pus formation may occur in shallow pockets, whereas deep pockets may exhibit little or no pus.
Localized accumulation of pus constitutes an abscess, which is discussed later in this chapter.
Root Surface Wall
The root surface wall of periodontal pockets often undergoes changes that are significant because they may perpetuate the periodontal infection, cause pain, and complicate periodontal treatment.
As the pocket deepens, collagen fibers embedded in the cementum are destroyed and ccmentum becomes exposed to the oral environment. Collagenous remnants of Sharpey's fibers in the cementum undergo degeneration, creating an environment favorable to the penetration of bacteria. Viable bacteria have been found in the roots of 87% of periodontals diseased noncarious teeth.1 Bacterial penetration into the cementum can be found as deep as the cementodentinal junction2'19 and may also enter the dentinal tubules (Fig. 22-15)."
Pathologic granules" have been observed with optical and electron microscopy" and may represent areas of collagen degeneration or areas where collagen fibrils have not been fully mineralized initially.
Penetration and growth of bacteria leads to fragmentation and breakdown of the cementum surface and result in areas of necrotic cementum, separated from the tooth by masses of bacteria (Fig. 22-16).
In addition, bacterial products such as endotoxins4' have also been detected in the cementum wall of periodontal pockets. When root fragments from teeth with periodontal disease .ire placed in tissue culture; they induce irreversible morphologic changes in the cells of the culture. Such changes are not produced by normal roots. Diseased root fragments also prevent the in vitro attachment of human gingival fibroblasts, whereas normal root surfaces allow the cells to attach freely.* When rcimplantcd in the oral mucosa of the patient, diseased root fragments induce an inflammatory response even if they are autoclaved.,,H
fhese changes are manifested clinically by softening of the cementum surface, which is usually asymptomatic but painful when a probe or explorer penetrates the area.
I hey also constitute a possible reservoir lor reinfection of the area after treatment. In the course of treatment, these nec rotic areas are removed by root planing until a hard smooth surface is reached. Cementum is very thin in the cervical areas, and scaling and root planing often removes it entirely, exposing the underlying dentin. Sensitivity to cold may result until secondary dentin is formed by the pulp tissue.
Fhe following changes may also occur in the root surface wall of periodontal pockets:
Decalcification and Kcmincrali/ation of Cementum. Areas of increased mineralization*** are probably
Fig. 22-15 Caries on roo! surfaces exposed by periodontal disease. A, Interdental space, showing inflamed gingiva and caries on proximal tooth surfaces. B, Caries ot cemenlum and dentin, showing bacterial inva sion of dentinal tubules. Note the filamentous structure of the dental plague and darker staining ol calculus adherent to the root.
Fig. 22-15 Caries on roo! surfaces exposed by periodontal disease. A, Interdental space, showing inflamed gingiva and caries on proximal tooth surfaces. B, Caries ot cemenlum and dentin, showing bacterial inva sion of dentinal tubules. Note the filamentous structure of the dental plague and darker staining ol calculus adherent to the root.
Fig. 22-16 Left, Mesiodistal section through an interdental space in a patient with extensive periodontal destruction. An area of cementum necrosis s enclosed within the rectangle designated by the arrow. Right, Detailed section of the rectangular area showing a necrotic fragment, ol cementum (C) separated Irom lamell.ited cementum (C) by clumps of bacteria (B).
Fig. 22-16 Left, Mesiodistal section through an interdental space in a patient with extensive periodontal destruction. An area of cementum necrosis s enclosed within the rectangle designated by the arrow. Right, Detailed section of the rectangular area showing a necrotic fragment, ol cementum (C) separated Irom lamell.ited cementum (C) by clumps of bacteria (B).
a result of an exchange, on exposure to the oral cavity, of minerals and organic components at the cementum-saliva interface. The mineral content of exposed cementum increases/'8 Hie following minerals are increased in diseased root surfaces: calcium, 1 magnesium, 11 phosphorus,54 and fluoride.54 Microtia rdness, however, re mains unchanged.*1"8* I he development of a highly mineralized superficial layer may increase the tooth resistance to decav. {
The hypermineralized zones arc detectable by electron microscopy and are associated with increased perfection of the crystal structure and organic changes suggestive ol a subsurface cuticle."*-0*' These zones have also been seen in microradiographic studies " as a layer 10 to 20 ¿¿m thick, with areas as thick as 50 /¿m. No decrease in mineralization was found in deeper areas, thereby indicating that increased mineralization does not come from adjacent areas. A loss of, or reduction in, the cross-handing of collagen near the ccmentum surface'0 w,and a subsurface condensation of organic material of exogenous origin*8 have also been reported.
Areas of demhterali/ation are commonly related to root caries, I \posure to oral fluid and bacterial plaque results in proteolysis of the embedded remnants of Sharpey's libers; the cementum may be softened and may undergo fragmentation and cavitation.38 Unlike enamel caries, root surface caries tend to progress around rather than into the tooth.Active root caries lesions appear as well-defined yellowish or light-brown areas, are frequently covered by plaque, and have a softened or leathery consistency on probing.26 Inactive lesions are well-defined darker lesions with a smooth surface and a harder consistency on probing.2''
The dominant microorganism in root surface caries is Actinomyces viscostts, although its specific responsibility in the development of the lesion has not been established." Other bacteria such as Actinomyces naeslundu, Streptococcus mutatis. Streptococcus sulivarius, Streptococcus sanguis, and Bacillus cereus have been found to produce root caries in animal models. Quirynen et alsx reported that when plaque levels and pocket depths fall after periodontal therapy (both conservative and surgical), a shift in oral bacteria occurs, leading to a reduction in periodontal pathogens and an increase iti S. mutatis and the development of root caries.
A prevalence rate study of root caries in 20- to 64-year-old individuals revealed that -12% had one or more root caries lesions and that these lesions tended to increase with age.41
The tooth may not be painful, but exploration of the root surface reveals the presence of a defect, and penetration of the involved area with a probe causes pain. Caries of the root, however, may lead to pulpitis, sensitivity to sweets and thermal changes, or severe pain. Pathologic exposure of the pulp occurs in severe cases. Root caries may be the cause of toothache in patients with periodontal disease and no evidence of coronal decay.
Caries of the ccmentum requires special attention when the pocket is treated. I he necrotic ccmentum must Ix? removed by scaling and root planing until firm tooth surface is reached, even if this entails extension into the dentin.
Areas of cellular resorption of ccmentum and dentin are common in roots unexposed by periodontal disease (see Figs. 2-16 and 22-16). ' These areas are of no particular significance because they are symptom free, and as long as the root is covered by the periodontal ligament, they are apt to undergo repair. However, if the root is exposed by progressive pocket formation before repair of such areas occurs, these appear as isolated cavitations that penetrate into the dentin. These areas can be differentiated from caries of the ccmentum by their clear-cut outline and hard surface. I hey may be sources of considerable pain, requiring the placement of a restoration.
Surface Morphology of the Tooth Wall of Periodontal Pockets. I his topic has been studied by several authors.* H The following zones can l>e found ift the bottom of a periodontal pocket dig. 22-17):
Calculus
Attached plaque
Unattached plaque
Junctional epithelium
Partially lysed c.t. fibers
Intact c t libers
Calculus
Attached plaque
Unattached plaque
Junctional epithelium
Partially lysed c.t. fibers
Fig. 22 17 Diagram of the area at the bottom of a pocket the Periodontal Pocket • UIAIMI.K 22 *47
1. Cementum covered by calculus, where all the changes described in the preceding paragraphs can be found.
2. Attached plaque, which covers calculus and extends apically from it to a variable degree, probably 100 to 500 /¿m.
3. The /one ol unattached phtiptc that surrounds attached plaque and extends apicalU lo it.
4. The zone where the junctional epithelium is iittacheil to the tooth. The extension of this /one. which in normal sulci is more than 500 /mi, is usually reduced in periodontal pockets to less than 100 /on.
5. Apical to the junctional epithelium, there may be ti /.one ofsemidestroyed connective tissue filters (see "Pathogenesis'').
Areas 3, 4, and 5 compose the so-called plaque-free 7.onc seen in extracted teeth. I he total width of the plaque-free zone varies according to the type of tooth (it is wider in molars than in incisors) and the depth of the pocket (it is narrower in deeper pockets).61 It is important to remember that the term plaque-free /one refers only to attached plaque because unattached plaque Kin-tains a variety of gram-positive cocci and various gram-negative morphotypes including cocci, rods, filaments, fusiforms, and spirochetes. I lie most apical /one contain predominantly gram-negative rods and cocci.8*1
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