JUNCTIONAL EPITHELIUM IN HEALTH & DISEASE-- REGENERATION FOLLOWING SURGERY
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This document provides an overview of junctional epithelium, including its structure, development, functions, and clinical significance. Some key points: - Junctional epithelium forms a collar around the tooth and attaches the gingiva. It is derived from reduced enamel epithelium during tooth development. - It has a stratified squamous non-keratinizing structure and rapidly turns over cells. The innermost layer of cells directly attach to the tooth surface. - It plays roles in passive eruption of teeth, acts as a barrier in gingivitis, and its conversion to pocket epithelium is a hallmark of periodontitis development. Loss of its attachment can lead to pocket formation and inflammation.
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JUNCTIONAL EPITHELIUM IN HEALTH & DISEASE-- REGENERATION FOLLOWING SURGERY
- 1. J U N C T I O N A L E P I T H E L I U M I N H E A LT H & D I S E A S E – R E G E N E R AT I O N F O L L O W I N G S U R G E R Y D R . A N T A R L E E N A S E N G U P T A I Y E A R M D S , D E P A R T M E N T O F P E R I O D O N T O L O G Y , M C O D S M A N G A L O R E 2 0 1 9 - 2 2 .
- 2. CONTENTS • INTRODUCTION • HISTORY • DEVELOPMENT OF JUNCTIONAL EPITHELIUM • STRUCTURE OF JUNCTIONAL EPITHELIUM • DYNAMIC ASPECTS • EXPRESSION OF VARIOUS MOLECULES & THEIR FUNCTIONS • CLINICAL SIGNIFICANCE OF JUNCTIONAL EPITHELIUM • BIOLOGIC WIDTH: CONCEPT & VIOLATION • REGENERATION OF JUNCTIONAL EPITHELIUM • CONCLUSION • REFERENCES 2
- 3. INTRODUCTION Junctional epithelium is the non-keratinizing stratified squamous epithelium, that surrounds the tooth like a collar with a cross- section resembling a thin wedge. Epithelium of the gingiva which gets attached to the tooth-- junctional or attachment epithelium. Derived from the reduced enamel epithelium (REE) during tooth development. Forms the floor of sulcus and attaches gingiva to tooth surface The union between this epithelium and tooth is referred to as epithelial attachment Resembles REE in its structure in that they have a basal layer and few layers of flattened cells OSE OEE CEJ JE 3
- 4. DEFINITION • The junctional epithelium consists of a collar like band of stratified squamous non- keratinizing epithelium. Joseph P. (Carranza’s 10th Edition) • A single or multiple layer of non- keratinizing cells adhering to the tooth surface at the base of the gingival crevice. [Glossary of Periodontal Terms] • The innermost cells of the junctional epithelium form and maintain a tight seal against the mineralized tooth surface. (Schroeder and Listgarten,1977) 4
- 5. HISTORY CONCEPTS ON JUNCTIONAL EPITHELIUM EXTEND OVER A PERIOD OF MORE THAN 90 YEARS Waerhaug (1960) Concept of epithelial cuff. Gingival tissue and tooth are closely adapted but not organically united. Gottlieb (1921) Epithelial attachment is organically united to the tooth surface Schroeder & Listgarten (1971) Primary & secondary epithelial attachment Waerhaug (1952) Cells of the epithelial attachment adhere weakly to tooth surface & forms lining of the physiologic pocket Orban (1953) Preparatory degenerative changes in the epithelium Listgarten (1966-67) Hemidesmosomal basement lamina attachment between the tooth & cells of the so- called epithelial attachment 5
- 6. 1971 • SCHROEDER et al 1976 • KOBAYASHI et al 1981 • STERN et al • SABAG et al Defined JE as- “the tissue that is affixed to the tooth on one side and to the oral sulcular epithelial and connective tissue on the other.” Unit of adhesion consisting of: - Sub Lamina Lucida (95 A) - Lamina Densa (400 A) - Lamina Lucida (140 A) & hemidesmosomes STERN et al: 400 A width of Lamina lucida (structure between outer leaflet of epithelial cell membrane and lamina densa) SABAG et al: attachment of epithelium to cementum surface is by 4-8 hemidesmosomes at coronal zone & 2 hemidesmosomes at apical zone of epithelial attachment. 6
- 7. DEVELOPMENT OF JUNCTIONAL EPITHELIUM 7
- 8. STRUCTURE OF JUNCTIONAL EPITHELIUM ANATOMICAL ASPECTS • Part of marginal free gingiva • Forms a collar peripheral to cervical region of tooth • In interproximal areas of adjacent teeth, fuse to form epithelial lining of COL • Coronal termination – free surface: – Pristine conditions: CEJ to gingival margin (~2 mm height) (Gargiulo et al, 1961) – Normal gingiva: subclinical inflammation (Brecx et al, 1987) – bottom of gingival sulcus • Apically & laterally – bordered by soft connective tissue – smooth surface; mild undulation coronally • Coronal-most – sulcular epithelium • Apical termination – IE in continuity with network of epithelial cell rests of Malassez. (Spouge, 1984) 8
- 9. STRUCTURE OF JUNCTIONAL EPITHELIUM JUNCTIONAL EPITHELIAL & INTERSTITIAL CELLS • Tapers off apically – Coronally: 15-30 cell layers – Apical termination: 1-3 cell layers • Stratified squamous non-keratinizing epithelium – Stratum Basale: cuboidal to slightly spindle- shaped – Stratum Suprabasale: flat, parallel to tooth surface, closely resemble each other – Innermost suprabasal cells– DAT cells(= directly attached to the tooth) (Salonen et al, 1989) -- these cells form and maintain the internal basal 9
- 10. DAT CELLS • Directly Attached to Tooth cells • The turnover of the junctional epithelium is exceptionally rapid. • At the coronal part of the JE, the DAT cells typically express a high density of transferrin receptors. • Any structural or molecular changes in the internal basal lamina can potentially influence the vital functions of the DAT cells and contribute to the effectiveness or failure of the junctional epithelial defense or vice versa. • Changes in the cell metabolism may affect the Internal Basal Lamina (IBL). 10
- 11. STRUCTURE OF JUNCTIONAL EPITHELIUM JUNCTIONAL EPITHELIAL & INTERSTITIAL CELLS • Lysosomal bodies– large numbers: contain enzymes that participate in eradication of bacteria • Golgi bodies- large • Abundant cisternae of RER • Polyribosomes- numerous. • Cytokeratin bundles- scarce. JE cells express a unique set of cytokeratins (5, 13, 14, 19 & weak activity for 8, 16, 18) • JE cells are interconnected by a few DESMOSOMES only, and occasionally by GAP JUNCTIONS. (Hashimoto et al., 1986) – remarkable permeability. • PMNs- central region of JE and near tooth surface • Lymphocytes & Macrophages- near basal cell layer • APCs, Langerhans cells, other dendritic cells (Juhl et al, 1988) 11
- 12. STRUCTURE OF JUNCTIONAL EPITHELIUM THE EPITHELIAL ATTACHMENT • JE faces both the gingival connective tissue(lamina propria) and the tooth surface. • Basal lamina – External basal lamina: interposed between basal cells of JE and gingival connective tissue – Internal basal lamina: forms part of the interfacial matrix between the tooth-facing junctional epithelial cells (DAT cells) and tooth surface – Continuous with basement membrane at apical end – specialized extracellular matrix – play roles in compartmentalization, filtration, cell polarization, migration, adhesion, and differentiation. 1. LAMINA LUCIDA or lamina rara 2. LAMINA DENSA 3. LAMINA FIBRORETICULARIS (sub-basal lamina) - Matrix constituents: collagen types IV and VII, laminin, heparan sulfate proteoglycan, fibronectin, Nidogen (entactin), Perlecan - The elements of the epithelial attachment are produced and renewed by the adjacent DAT cells (Osman and Ruch, 1980) and, hence, are part of the dynamics of the junctional epithelium. 12
- 13. DYNAMIC ASPECTS OF JUNCTIONAL EPITHELIUM • JE cells are essential for protective & regenerative functions • High cellular turnover (Demetriou & Ramfjord, 1972) • Exfoliation of daughter cells occurs in the free surface of JE • Cells migrate coronally towards free surface to DESQUAMATE– exfoliation occurs at extremely high rate (Listgarten, 1972) • Cell mitosis occurs in basal and DAT cells (Salonen, 1994) • DAT cells– – migrate towards the sulcus bottom – Connected via hemidesmosomes to basal lamina → not static but dynamic • Intercellular spaces of JE– pathway for fluid & transmigrating leukocytes • In the absence of clinical signs of inflammation, approximately 30,000 PMNs migrate per minute through the junctional epithelia of all human teeth into the oral cavity (Schiött and Löe, 1970). 13
- 14. EXPRESSION OF VARIOUS MOLECULES & THEIR FUNCTIONS IL-8 IL-1 TNF INTEGRINS CADHERINS CEA-CAM ICAM-1 LFA-3 Tonetti et al, 199814
- 16. ROLE OF JE IN PASSIVE ERUPTION 16
- 17. ROLE OF JE IN PASSIVE ERUPTION Stage 1: The teeth reach the line of occlusion. The junctional epithelium and base of the gingival sulcus are on the enamel. 17
- 18. ROLE OF JE IN PASSIVE ERUPTION Stage 2: The junctional epithelium proliferates so that part is on the cementum and part is on the enamel. The base of the sulcus is still on the enamel. 18
- 19. ROLE OF JE IN PASSIVE ERUPTION Stage 3: The entire junctional epithelium is on the cementum, and the base of the sulcus is at the cementoenamel junction. As the junctional epithelium proliferates from the crown onto the root, it does not remain at the cementoenamel junction any longer than at any other area of the tooth. 19
- 20. ROLE OF JE IN PASSIVE ERUPTION Stage 4: The junctional epithelium has proliferated farther on the cementum. The base of the sulcus is on the cementum, a portion of which is exposed. Proliferation of the junctional epithelium onto the root is accompanied by degeneration of gingival and periodontal ligament fibers and their detachment from the tooth. The cause of this degeneration is not understood. At present, it is believed to be the result of chronic inflammation and therefore a pathologic process. 20
- 21. ROLE OF JE IN GINGIVITIS 21
- 22. ROLE OF JE IN POCKET FORMATION • Conversion of JE to pocket epithelium is regarded as the hallmark in the development of periodontitis Inflammation Supracrestal collagen destruction Lossofcontactinhibition, Over-expressionofEGF Apical migration of JE Inflammatorycellinfiltration Coronal detachment of JE • pooling of inflammatory cells • Degeneration of cell adhesion molecules • Destruction of cell adhesion complexes • Loss of contact inhibition • Increased expression of EGF and its receptors • no internal and external basal lamina 22
- 23. ROLE OF JE IN POCKET FORMATION Several researchers have attributed pocket formation to a Loss of cellular continuity in the coronal-most portion of the junctional epithelium, implicating detachment of the DAT cells from the tooth surface or to the development of an intra-epithelial split. (Schluger et al., 1977; Schroeder and Listgarten, 1977) Degenerative changes in the second or third cell layer of the DAT cells in the coronal-most portion of the junctional epithelium facing the bacterial biofilm. (Takata and Donath,1988) With increasing degrees of gingival inflammation, both the emigration of PMNs and the rate of gingival crevicular fluid passing through the intercellular spaces of the junctional epithelium increase. (Kowashi et al., 1980) Increased number of mononuclear leukocytes contribute to the focal disintegration of the junctional epithelium. (Schroeder and Listgarten, 1997) 23
- 24. ROLE OF JE IN POCKET FORMATION • Pocket formation is the result of subgingival spreading of bacteria under impaired defense conditions (Schroeder and Attström, 1980). • Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis (P. gingivalis) (Quirynen et al., 2001) • GINGIPAINS– cysteine proteinases-- virulence factors produced by P. gingivalis (Imamura, 2003). – specifically degrade components of the epithelial cell-to-cell junctional complexes (Hintermann et al., 2002). – immune evasion mechanism by P. gingivalis – disintegration of the junctional epithelium (Tada et al., 2003). – Epithelial cells exhibit • proteolysis of focal contact components, • adherens junction proteins, and • adhesion signaling molecules 24
- 25. EFFECT OF TRAUMA FROM OCCLUSION ON JE • TFO causes widening of the marginal PDL space, a narrowing of the interproximal alveolar bone. • In case of TFO, the junctional epithelium will be intact and there will be no degeneration of the epithelial tissues unless there is any plaque accumulation. 25
- 26. JE AROUND IMPLANTS • Junctional epithelium around implants always originates from epithelial cells of oral mucosa. • Despite different origins of the 2 epithelia, a functional adaptation occurs when oral epithelia form an epithelial attachment around implants. NATURAL TOOTH Epithelium tapers towards the depth Large number of cell organelles Fibers are arranged perpendicular IMPLANT Epithelium is thicker Few organelles Fibers are arranged parallely Numerous kerato- hyalin granules (Atsuta et al, 2016) 26
- 27. JE AROUND IMPLANTS • Evidence of several of the mentioned marker molecules involved in the defense mechanisms against the bacterial also being expressed in the peri-implant epithelium. 27
- 28. BIOLOGIC WIDTH:The dimension of the space that the healthy gingival tissue occupies above the alveolar bone is called the biologic width (Gargiulo et al., 1961) CONCEPT & VIOLATION • Margin placement. • Margin adaptation. • Restoration contour. • Occlusal function. Direct causative effect on biological width 28
- 29. BIOLOGIC WIDTH: CONCEPT & VIOLATION VIOLATION OF BIOLOGIC WIDTH: • restoration of a tooth that has fractured or been carious near the alveolar crest. • esthetic concerns– subgingival placement of restoration margins: into the gingival sulcus The signs of biologic width violation are: • Chronic progressive gingival inflammation around the restoration. • Bleeding on probing. • Localized gingival hyperplasia with minimal bone loss. • Gingival recession. • Pocket formation. • Clinical attachment loss. • Alveolar bone loss. • Gingival hyperplasia (most frequently found in altered passive eruption and subgingivally placed restoration margins). 29
- 30. BIOLOGIC WIDTH:CONCEPT & VIOLATION METHODS TO DETECT BIOLOGICAL WIDTH VIOLATION BONE SOUNDING/ TRANSGINGIVAL PROBING RADIOGRAPHIC EVALUATION A. B. (CARRANZA 10TH Edn., 2006) (Galgali et al., 2011) 30
- 31. SYNDROMES AFFECTING JE • Haim-Munk syndrome and Papillon-Lefèvre syndrome due to allelic mutations in cathepsin C. JE gives rise to episodic inflammation and destruction of gingiva. (Hart al, 2000) • Kindler syndrome: due to loss of kindlin-1 protein which is involved in integrin activation. A rare skin blistering disorder along with early onset aggressive periodontitis. JE fails to attach to the tooth surface. (Yildirim et al, 2017) 31
- 33. BIOLOGY OF PERIODONTAL REGENERATION “Type of cell which repopulates the root surface after periodontal surgery determines the nature of the attachment that will form.” (MELCHER, 1973 SR) • Epithelial cells • Cells derived from the gingival connective tissue • Cells derived from the bone • Cells derived from the periodontal ligament. 33 POSSIBLE OUTCOMES OF PERIODONTAL THERAPY
- 34. • In humans, a new junctional epithelium after gingivectomy may form within 20 days (Schroeder and Listgarten, 1977). • Waerhaug (1981): Detachment of cells persisted for 24 hrs after flossing ceased. New attachment of junctional epithelial cells started 3 days after flossing ceased. After 2 wks, the cell populations on the experimental and control surfaces were again indistinguishable from each other. • Clinical probing results in a mechanical disruption of the junctional epithelial cells from the tooth. The reestablishment of the epithelial seal around implants after clinical probing was shown to occur within about the same time period (Etter et al., 2002). • These studies show that the junctional epithelium is a highly dynamic and adaptive with a fast capacity for self renewal or de novo formation from basal cells of the oral gingival epithelium. 34
- 35. C O N C L U S I O N 35 The junctional epithelium is a unique tissue that fulfills a challenging function at the border between the oral cavity, colonized by bacteria, and the tooth attachment apparatus. These defense mechanisms may be overwhelmed by bacterial virulence factors, and the gingival lesion could progress to periodontitis. Recent studies have shed light on the role of gingipains in this process. Such new information may be used to develop therapeutic strategies aimed at neutralizing the detrimental effects of these cysteine proteinases.
- 36. R E F E R E N C E S 1. Clinical Periodontology – CARRANZA 10th Edn. 2. Periodontal diseases -- SCHLUGER 2nd edn. 3. Oral Histology -- ORBAN 10th edn. 4. Oral Histology – TENCATE 6th edn. 5. Periodontology 2000 vol. 13, 1997 6. AAP. Periodontal Literature Review – 1996. 7. Bosshardt DD, Lang NP. The junctional epithelium: from health to disease. Journal of dental research. 2005 Jan;84(1):9-20. 8. Aishwarya M, Sivaram G. Biologic width: Concept and violation. SRM Journal of Research in Dental Sciences. 2015 Oct 1;6(4):250. 9. Moon-Il Cho & Philias R. Garant. Development and general structure of the periodontium. Periodontology 2000, Vol. 24, 2000, 9–27. 10. Mark Bartold, Laurence J. Walsh & A. Sampath Narayanan. Molecular and cell biology of the gingiva.P. Periodontology 2000, Vol. 24, 2000, 28–55. 11. Huberte . Schroede & R M Listgarten. The gingival tissues: The architecture of periodontal Protection. Periodontology 2000, Vol. 13, 1997, 91-120. 12. Takashi Sawada1 and Sadayuki Inoue. Ultrastructure of Dentogingival Border of Normal and Replanted Tooth and Dental Implant, chapter 11 www.intechopen.com/books/implantdentistry 36
- 37. THANK YOU
Editor's Notes
- The term epithelial attachment: refers to the attachment apparatus, i.e. the internal basal lamina and hemidesmosomes, that connects the junctional epithelium to the tooth surface. This term is not synonymous with attachment epithelium which refers to the entire epithelium. (basal, suprabasal membranes and other cell layers) - There are 3 types of mucous membranes masticatory, lining, and specialized that line the oral cavity and form the structural boundary between the body and the external environment. It is commonly accepted that the junctional epithelium exhibits several unique structural and functional features that contribute to preventing pathogenic bacterial flora from colonizing the subgingival tooth surface. Epithelia exhibit considerable differences in their histology, thickness and differentiation suitable for the functional demands of their location The gingival epithelium around a tooth is divided into three functional compartments– outer, sulcular, and junctional epithelium The outer epithelium extends from the mucogingival junction to the gingival margin where crevicular/sulcular epithelium lines the sulcus At the base of the sulcus connection between gingiva and tooth is mediated with JUNCTIONAL EPITHELIUM . It is bounded CORONALLY by the free gingival groove and APICALLY by the mucogingival junction •
- The term epithelial attachment: refers to the attachment apparatus, i.e. the internal basal lamina and hemidesmosomes, that connects the junctional epithelium to the tooth surface. This term is not synonymous with attachment epithelium which refers to the entire epithelium. (basal, suprabasal membranes and other cell layers)
- 2. Based on his animal experiments(in dogs) he postulated that 3. Separation of epithelial attachment cells from tooth surface involved 4. This concept was based on insertion of thin blades between the surface of tooth and the gingiva. Blades could be easily passed apically to the connective tissue attachment at CEJ without resistance. 5. Based on transmission electron microscopic studies he proved the existence of a 6. Primary epithelial attachment refers to the epithelial attachment lamina released by the REE. It lies in direct contact with enamel and epithelial cells attached to it by hemi-desmosomes. When REE cells transform into JE cells the primary epithelial attachment becomes secondary epithelial attachment. It is made of epithelial attachment between basal lamina and hemi-desmosomes.
- KOBAYASHI studied JE of monkeys, reporting a highly variable relationship b/w junctional epi and tooth surface coronal to CEJ.
- When the enamel of the tooth is fully developed, the enamel‐producing cells (ameloblasts) become reduced in height, produce a basal lamina, and form, together with cells from the outer enamel epithelium, the so‐called reduced dental epithelium(RE). The basal lamina (epithelial attachment lamina [EAL]) lies in direct contact with the enamel. The contact between this lamina and the epithelial cells is maintained by hemidesmosomes. The reduced enamel epithelium surrounds the crown of the tooth from the moment the enamel is properly mineralized until the tooth starts to erupt. As the erupting tooth approaches the oral epithelium, the cells of the outer layer of the reduced dental epithelium (RE), as well as the cells of the basal layer of the oral epithelium (OE), show increased mitotic activity (arrows) and start to migrate into the underlying connective tissue. The migrating epithelium produces an epithelial mass between the oral epithelium and the reduced dental epithelium so that the tooth can erupt without bleeding. The former ameloblasts do not divide. When the tooth has penetrated into the oral cavity, large portions immediately apical to the incisal area of the enamel are covered by a junctional epithelium (JE) containing only a few layers of cells. The cervical region of the enamel, however, is still covered by ameloblasts (AB) and outer cells of the reduced dental epithelium. During the later phases of tooth eruption, all cells of the reduced enamel epithelium are replaced by a junctional epithelium (JE). This epithelium is continuous with the oral epithelium and provides the attachment between the tooth and the gingiva. If the free gingiva is excised after the tooth has fully erupted, a new junctional epithelium, indistinguishable from that found following tooth eruption, will develop during healing. The fact that this new junctional epithelium has developed from the oral epithelium indicates that the cells of the oral epithelium possess the ability to differentiate into cells of the junctional epithelium.
- Free surface- located at bottom of sulcus, at gingival margin, or interdental col area. FIGURE: light microscopic view of human gingiva: ABC alveolar bone crest AEFC acellular extrinsic fibrillar cementum CEJ cemento enamel junction CT connective tissue D dentin ES enamel space GM gingival margin JE junc epi OGE oral gingival epithelium OSE oral sulcular epi PL pdl ligament
- Free surface- located at bottom of sulcus, at gingival margin, or interdental col area. FIGURE: light microscopic view of human gingiva: ABC alveolar bone crest AEFC acellular extrinsic fibrillar cementum CEJ cemento enamel junction CT connective tissue D dentin ES enamel space GM gingival margin JE junc epi OGE oral gingival epithelium OSE oral sulcular epi PL pdl ligament Basal cells face the gingival conn tissue SEM image showing the apical tapering of JE A schematic illustration of a DAT cell shows the structural and molecular composition of the epithelial attachment apparatus (EAA). N = nucleus of a DAT cell, IF = cytoplasmic keratin filaments (intermediate size filaments). The hemidesmosomes at the plasma membrane are associated with the a6b4 integrin that communicates with Ln-5 = laminin 5 located mainly in the internal basal lamina, the extracellular domain (?) for BP180 is a collagenous protein (perhaps type VIII), that has not yet been definitely characterized. LL =lamina lucida, LD =lamina densa, SLL =sublamina lucida, IBL = internal basal lamina.
- DAT cells have more important role in tissue dynamics and reparative capacity of the junctional epithelium than has previously been thought. The mechanism of DAT cell turnover is not fully understood. Considering the fact that the DAT cells are able to divide and migrate, three possible mechanisms can be proposed. These are TURNOVER MECHANISM the daughter cells produced by dividing DAT cells replace degenerating cells on the tooth surface, the daughter cells enter the exfoliation pathway and gradually migrate coronally between the basal cells and the DAT cells to eventually break off into the sulcus, or epithelial cells move/migrate in the coronal direction along the tooth surface and are replaced by basal cells migrating round the apical termination of the junctional epithelium.
- Transmission electron micrograph illustrating desmosomes (DES) and cytokeratin filaments (CK) in the junctional epithelium from a human tooth with a clinically healthy gingiva. N, nucleus of a junctional epithelial cell.
- LAMINA LUCIDA or lamina rara: basal lamina hemidesmosomes consist of an attachment plaque associated with cytokeratin filaments and the sub-basal dense plate, which is extracellularly located in the lamina lucida LAMINA DENSA: directly faces the enamel, dentin, or cementum (fibrillar or afibrillar) LAMINA FIBRORETICULARIS (sub-basal lamina): forms a discontinuous layer consisting of reticular and anchoring fibrils Internal basal lamina of the junctional epithelium has its own characteristics and cannot be regarded as a basement membrane in the true sense. TEM image: basal lamina consisting of lamina lucida and lamina densa and hemidesmosomes at the interface b/w JE and tooth. The interposed matrix layer may be a dental cuticle or a modified cementum specialized extracellular matrices interposed between connective tissues and epithelia, endothelia, muscle fibers, and the nervous system play roles in compartmentalization (physical barrier function), filtration (selective permeability barrier function or molecular sieve function), cell polarization, migration, adhesion, and differentiation.
- The tissue fluid transports a variety of molecules through the junctional epithelium to the bottom of the gingival sulcus. These molecules, together with the leukocytes, represent a host defense system against the bacterial challenge. Thus, gingival fluid is an exudate that originates from the subepithelial blood vessels of the lamina propria, and its flow rate corresponds to the degree of inflammation. Thus justifying the implication that gcf is an exudate in cases of inflammation
- Knowledge about structure and molecules involved in the maintenance of cell-cell contact is particularly important in view of the pathological changes that the epithelium undergoes during its conversion to a pocket lining. IL-8, IL-1, TNF: Chemotaxis; guiding PMNs toward the sulcus bottom. innate immune defense Integrins: cell surface receptors that mediate interactions between cell and extracellular matrix, and also contribute to cell to cell adhesion. Cells in contact with the internal basal lamina (adjecent to enamel) express the integrins. CADHERINS: esponsible for tight contacts between cells. E-cadherin, an epithelium specific cell adhesion molecule, plays a crucial role in maintaining the structural integrity. CEA-CAM: carcino-embryogenic Ag related cell adhesion molecule – guidance of PMNs through JE, proliferation, stimulation & co- regulation of T- Cells. - Odin et al & Öbrink et al ICAM-I: Intercellular adhesion molecule – 1. cell-cell interactions in inflammatory reactions- Crawford and Hopp LFA-3: Lymphocyte function antigen-3 (LFA-3). controls leukocyte migration to inflammatory site - Crawford
- This concept distinguishes between the anatomic crown (the portion of the tooth covered by enamel) and the anatomic root (the portion of the tooth covered by cementum) and between the clinical crown (the part of the tooth that has been denuded of its gingiva and projects into the oral cavity) and clinical root (the portion of the tooth covered by periodontal tissues). When the teeth reach their functional antagonists, the gingival sulcus and junctional epithelium are still on the enamel and the clinical crown is approximately two-thirds of the anatomic crown. Passive eruption is the exposure of the teeth by apical migration of the gingiva. Passive eruption is divided into four stages. Although this was originally thought to be a normal physiologic process, it is now considered a pathologic process.
- LINDHE 1973 experimental plaque-induced periodontitis in beagle dog model, Journal Perio Research Initial lesion: Leukocytes, mainly PMN leukocytes leave the capillaries by migrating through the walls (Lindhe, 1973). They can be seen in increased quantities in the connective tissue, and the junctional epithelium and the gingival sulcus. Early lesion: The junctional epithelium becomes densely infiltrated with neutrophils and it may begin to show development of rete pegs or ridges. Established lesion of gingivitis: The junctional epithelium reveals widened intercellular spaces filled with granular cellular debris, including lysosomes derived from disrupted neutrophils, lymphocytes and monocytes. JE forms rete pegs or ridges that protrude into the connective tissue and the basal lamina is destroyed in some areas.
- JE in pockets are slightly shorter APICAL MIGRN: Due to- Loss of contact inhibition -due to supra crestal collagen destruction Increased expression of EGF and its receptors due to cytokine stimulation Epithelial cell at apical end of migrating JE have no internal and external basal lamina CORONAL DETACHMENT: Due to More pooling of inflammatory cells at the coronal end Degeneration of cell adhesion molecules by inflammatory mediators Destruction of cell adhesion complexes directly by bacterial enzymes such as gingipains
- 2. Similar observations were made in a dog model (Hillmann et al., 1990). Several attempts to explain the reason for the cleavage within the junctional epithelium have been made. 3. Moderately distended intercellular spaces are not considered to interfere with the structural and functional integrity of the junctional epithelium (Schroeder and Listgarten, 1997). However, an
- JE-- 'open system' -- allows cells and substances to emigrate from the gingival connective tissue into the sulcus, thereby clearing and counteracting the continuous bacterial challenge Particular attention has been paid to elucidating the mechanisms by which A.a and P.g, 2 pathogens implicated as major etiological agents in aggressive and chronic periodontitis, adhere to, invade, and replicate in epithelial cells Gingipains have been the focus of research over the last few years Thus, bacterial products penetrating the junctional epithelium at the bottom of the sulcus may directly perturb the structural and functional integrity of the junctional epithelium. The proteolytic disruption of the epithelial integrity may not only be a significant factor in the initiation of pocket formation, but may also pave the way for bacterial invasion into the subepithelial connective tissue in advanced stages of the lesion.
- As opposed to JE around teeth which rises from REE. The JE around tooth is characterized by a wide intercellular space, because JE is a non-keratinized epithelium that has only weak cell-to-cell contacts and is affected by exogenous factors. Peri-implant junction is composed of three types of epithelium: peri-implant epithelium (PIE), peri-implant sulcular epithelium (PISE), and oral epithelium (OE).
- Peri-implant junction is composed of three types of epithelium: peri-implant epithelium (PIE), peri-implant sulcular epithelium (PISE), and oral epithelium (OE). In addition, there is a biologic width of 3–4 mm around implant, slightly longer than that around natural tooth. The PIE performs a similar epithelial attachment function to the JE, and forms from the OE within 2–3 weeks after implantation. Morphologically, PIE is composed of a thin layer of 3–4 cells, and has immunoglobulins, neutrophils, lumphocytes and plasma cells, in a wide intercellular space, which together protect the underlying tissue from deleterious exogenous factors. However, despite oral mucosa contacting both the implant abutment and implant body immediately after placement, the PIE often ultimately contacts only the implant body because of on-going bone resorption around the implant as the implant-abutment interface becomes a cause of inflammation. Because of the shifting nature of this bone level, it is challenging to predict the condition of the gingiva after implant surgery. Furthermore, the PIE has a much lower functional sealing capacity than JE, despite having very similar epithelial structures. The lower adhesion of the OE to titanium seems to be caused by the electrostatic characteristics of the implant and ion elution, but the precise reason remains unclear.
- Biologic width is essential for — the preservation of periodontium and removal of irritation that might damage the periodontium. The dimension of biologic width is not constant, it depends on the location of the tooth in the alveolar, varies from tooth to tooth, and also from one surface of the tooth to another. Violation of the biologic width — leads to ultimate failure of the restoration.
- Violation of the biologic width — leads to ultimate failure of the restoration. If a patient experiences tissue discomfort when the restoration margin levels are being assessed with a periodontal probe, it is a good indication that the margin extends into the attachment and that a biologic width violation has occurred.
- BONE SOUNDING: The biologic width can be identified by probing under local anesthesia to the bone level (referred to as “sounding to bone”) and subtracting the sulcus depth from the resulting measurement. If this distance is <2 mm at one or more locations, a diagnosis of biologic width violation can be confirmed. RADIO EVAL: Radiographic interpretation can identify interproximal violations of biologic width. However, on the mesiofacial and distofacial line angles of teeth, radiographs are not diagnostic because of tooth superimposition. Parallel profile radiographic technique has been devised which could be used to measure both length and thickness of the dentogingival unit with accuracy. * The health of periodontal tissue is dependent on properly designed restoration. Incorrectly placed restorative margins and poorly adapted restorations violate the biologic width, an in turn, influence the junctional epithelium adequacy as well.
- New attachment with periodontal regeneration is the ideal outcome of therapy because it results in obliteration of the pocket and reconstruction of the periodontium . However, the techniques available are not totally dependable, and other therapeutic results may be seen depending on the type of cell. After flap surgery the curetted root surface may be repopulated by 4 different types of cells: PERIODONTAL WOUND HEALING if the epithelium proliferates along the root surface before other tissues reach the area, the result will be long junctional epithelium. if the cells from gingival connective tissue are first to populate the area, result will be fibers parallel to the tooth surface & remodelling of alveolar bone with no attachment to the cementum. if bone cells arrive first, root resorption & ankylosis may occur. When cells from the periodontal ligament proliferate coronally, there is new formation of cementum & periodontal ligament.
- In the above studies, the junctional epithelium was never completely removed from the tooth. However, the application of gingivectomy techniques would completely remove the junctional epithelium. Subsequently, the formation of a new junctional epithelium must occur from basal cells of the oral gingival epithelium (Braga and Squier, 1980). Since the junctional epithelium is located at a strategically important but also delicate site, it may be expected that it should be very well-adapted to cope with mechanical insults Whether and how fast a new epithelial attachment reforms have been the objectives of several studies. In an experimental study in marmosets, following probing, a new and complete attachment indistinguishable from that in controls was established 5 days after complete separation of the junctional epithelium from the tooth surface (Taylor and Campbell, 1972). In both studies, persistence of tissue trauma and infection as a result of probing were not observed. Based on these 2 studies, probing around teeth and implants does not seem to cause irreversible damage to the soft tissue components. Oral hygiene practices may be accompanied by undesired trauma to the junctional epithelium as well.
- There is a constant presence of bacteria and their products in the gingival sulcus which makes this an important structural component of periodontal defense mechanism. Bacteria, such as, e.g., P. gingivalis, may directly perturb the structural and functional integrity of the junctional epithelium.