Gingiva in health and disease

this presentation holds up maximum information on gingiva in health and disease

1. Dr. Lakkireddy Vasavi reddy Gingiva in health and disease

2. Contents:

3. Introduction:

4. Definition:

5. Macroscopic features: The gingiva is divided anatomically into Marginal Attached Interdental areas.

6. Marginal gingiva It is unattached gingiva, which is the terminal edge or border of the gingiva surrounding the teeth in collar like fashion. It is about 1mm wide, it forms the soft tissue wall of the gingival sulcus Free gingival groove -In about 50% cases, marginal gingiva is demarcated from the adjacent, attached gingiva by a shallow linear depression, runs parallel to & at a distance of 0.5 to 2mm from the margin of gingiva. It may be separated from the tooth surface with a periodontal probe.

7. Gingival sulcus: “It is shallow crevice or space around the tooth bounded by the surface of the tooth on one side and the epithelium lining the free margin of the gingiva on the other.” It is “V” shaped and barely permits the entrance of a periodontal probe. Histological depth- 1.8mm with variations from 0 to 6mm, other studies have reported 1.5mm and 0.69mm, respectively. Probing depth - normal gingival sulcus is 2 to 3 mm. Ideal condition- 0mm

8. Development of gingival sulcus:

9. Attached gingiva It is firm resilient and tightly bound to the underlying periosteum of alveolar bone. Width of attached gingiva “It is the distance between the mucogingival junction and the projection on the external surface of the bottom of the gingival sulcus or the periodontal pocket.” Greatest in the incisor region -3.5to4.5mm in maxilla, 3.3to3.9mm in mandible Least in first premolar area -1.9mm in maxilla , 1.8mm in mandible

10. Methods for assessing attached gingiva

11. FUNCTIONS: Dissipates functional and masticatory stresses. Provides a resistant barrier to plaque induced inflammation. Prevents deflection of marginal gingiva due to effects of frena & lip musculature. Aids in plaque maintenance & ease of oral hygiene maintenance. Improves aesthetics.

12. Studies:

13. Andlin-Sobocki and Bodin (1993)

14. Voigt et al.

15. Width of attached gingiva:

16. Eager divided attached gingiva based on periodontal type:  Shallow thin gingiva with slender crown formation.  Wide thick gingiva with quadrant crown formation.  Unknown combination   TISSUE BARRIER CONCEPT: Goldman and Cohen outlined a “tissue barrier” concept for mucogingival surgery. They postulated that a dense Collagenous band of connective tissue retard or obstruct the spread of inflammation better than does the loose fiber arrangement of the alveolar mucosa. They recommended increasing the zone of keratinized tissue to achieve an adequate tissue barrier

17. Thickness of Free and Attached Gingiva

18. Interdental papilla: The interdental gingiva occupies the gingival embrasure, which is the interproximal space beneath the area of the tooth contact. Col shape is because it represents the valley like depression that connects a facial & lingual papilla and conforms to the shape of the interproximal contact.

19. In a study using Rhesus monkeys, McHugh (1974) confirmed that the interdental area is col-shaped. This area consists of soft tissue residing between papillary peaks on the buccal and lingual. Histological analysis of sections through the actual col showed that it is always lined by squamous epithelium, 5 or more cell-layers thick. Ameloblasts were not found.

20. Microscopic features: Gingival epithelium: stratified squamous epithelium 0.2-0.3mm in thickness Subdivided into different layers on the basis of degree of keratin production.

21. Gingival epithelium:

22. Keratinocyte: Major cell type of the gingival epithelium. Proliferation: by mitosis in basal layer; less frequently in supra basal layers. Differentiation: involve process of keratinization. Progressions of biochemical and morphological events that occur as cell migrate from basal layer to S. corneum.

23. Keratinization:

24. Keratin expression:

25. Non keratinocytes: MELANOCYTES: Present in basal and spinous layers. Stellate cells with numerous dendritic processes. Synthesise melanin in premelanosomes or melanosomes. Attached neither to the subjacent basal lamina nor to adjacent cells of the stratum basale. Contain tyrosinase which hydroxylates tyrosine to dihydroxy-phenylalanine (DOPA ) which in turn is converted to melanin. Melanin granules are phagocytosed and contained within melanophages or melanophores.

26. Langerhans cells Dendritic cells located among keratinocytes at all suprabasal levels belong to mononuclear phagocyte system (R.E system). Considered macrophages with possible antigenic properties, important role in immune reaction as antigen-presenting cells for lymphocytes. Contain g-specific granules( Birbeck’s granules) and have marked adenosine triphosphatase activity. Found in oral epithelium of normal gingiva and in smaller amounts in the sulcular epithelium probably absent from the junctional epithelium of normal epithelium.

27. Merkel cells Located in the deeper layers of the epithelium, harbour nerve endings and are connected to the adjacent cells by desmosomes. They have been identified as tactile preceptors.

28. Structure and metabolic characteristics: The epithelium covering the gingiva may be differentiated as follows: • oral epithelium (OE), which faces the oral cavity. • oral sulcular epithelium (OSE), which faces the tooth without being in contact with the tooth surface. • junctional epithelium (JE), which provides the contact between the gingiva and the tooth.

29. Oral(outer) epithelium Covers crest & outer surfaces of marginal gingiva & surface of attached gingiva . Keratinized or parakeratinized or various combinations with prevalence toward parakeratinization . Keratinization varies in following order: Palate(Most keratinized)> Gingiva>Ventral aspect of Cheek(Least keratinized)

30. Stratum basale: the cells – cylindrical / cuboidal Attached to underlying basement membrane and to each other by hemidesmosomes and gap junctions. Cells have ability to undergo mitosis. Also called as stratum germinativum . ( progenitor cell compartment of epithelium) Consists of keratinocytes, melanocytes .

31. Stratum spinosum: Uppermost layers contains Odland bodies or keratinosomes. Contain fewer cell organelles and more tonofibrils. Expression of K1 & K10 increases. Expression of K5 & K14 decreases. Keratin bundles increase in number. Cell to cell attachment - desmosomes. Gap junctions - high numbers. Langerhans cells are present

32. Stratum granulosam: Cells become flattened. Named because of keratohyaline granules. They are 1 to 0.1 µm in diameter round or irregular and electron dense, present in cytoplasm and stain with acid dyes (haemotoxylin) Nuclei shows signs of degeneration. Tonofibrils more prominent. Sythesizes protein. Desmosomes becomes oriented.

33. Stratum corneum Cells undergo transition. Increased tonofilaments Cell organelles, keratohyaline granules disappear. Consists of flat cells termed squame (stain pink with eosin). Densely packed filaments – keratins(K1,K2,K10,K12) ; covered by filaggrin layer (envelope). Crosslinking of tonofilaments – disulphide bonds – mechanical strength & chemical resistance.

34. Basal lamina 300 – 400 Å thick. Approx. 400 Å beneath basal layer of epithelium. Permeable to fluids. Barrier to particulate.

35. Sulcular epithelium: It is a thin, nonkeratinized stratified squamous epithelium without retepegs and extends from coronal limit of the junctional epithelium to the crest of the gingival margin.  It lacks granulosum & corneum strata and normally does not contain Merkel cells. It has potential to keratinize if -exposed to oral cavity -bacterial flora is eliminated. It suggests that local irritation of sulcus prevents sulcular keratinization. Importance It may act as a semipermeable membrane though which injurious bacterial products pass into the gingiva and tissue fluid from gingiva seeps into the sulcus

36. Junctional epithelium: A single or multiple layer of non-keratinizing cells adhering to the tooth surface at the base of the gingival crevice. Formerly called epithelial attachment. Length : 0.25 to 1.35mm Thickness: 3 – 4 cell layer in early life. 10 – 29 cell layers – coronal 1 - 2 cell layers – apical

37. Concepts:

38. Schroeder & Listgarten Prior to eruption, the surface of the enamel is covered by the REE which comprises the reduced ameloblasts and the former stratum intermedium. These cells produce a basal lamina called the epithelial attachment lamina, which is in contact with the hard tissue structure. It is to this lamina that the epithelial cells attach, via hemidesmosomes, to form the primary epithelial attachment in unerupted teeth. As tooth erupts, the reduced ameloblasts and some cells of the stratum intermedium get converted into junctional epithelial cells. As the tooth erupts through the oral mucosa, the attachment of soft to hard tissue is termed the secondary epithelial attachment , which may consist simply of a basal lamina (the epithelial attachment lamina) anhemidesmosomes

39. Dynamic aspects of junctional epithelium: Turnover is very high  protective & regeneration Earlier thought epithelial cells facing external basal lamina divide rapidly. proteoglycans , hyaluronan , decorin , syndecan and CD-44…on epithelial cell surfaces and within intercellular spaces. β 1 integrin family and intercellular adhesion molecule-1….. Cell adhesion Evidence  DAT cells high mitotic activity DAT cells  Role in tissue dynamics & reparative capacity of JE.

40. DAT cells: Daughter cells replace degenerating cells on tooth surface Daughter cells enter exfoliation pathway & gradually migrate coronally between basal cells & DAT cells Epithelial cells move in coronal direction along tooth surface

41. Renewal of gingival epithelium: Skougaard and Beagrie (1962) investigated renewal time in the gingival epithelium of marmosets using injections of tritiated thymidine and autoradiography. Epithelial cells in the attached gingiva exhibited a renewal rate of 10.4 days, whereas the corresponding rate for the epithelial cuff was 5.8 days

42. Cuticular structures of tooth: Cuticle describes a thin acellular structures with homogenous matric that is sumtimes enclosed within clearly demarcated linear borders. Listgarten divided the as: Acquired – saliva, bacteria, calculus and surface stains Developemtal origin- REE, coronal epithelium, dental cuticle

43. Gingival connective tissue: 60% - collagen fibres , 5%- fibroblasts, 35%- vessels, nerves & matrix. Also known as LAMINA PROPRIA. Papillary layer Reticular layer Sub adjacent to epithelium; consists of papillary projections between epithelial rete pegs. Density - 120+30/mm2 gingival surface. Contiguous with the periosteum of the alveolar bone.

44. Cellular elements:

45. Fibroblast: 65% of cells of gingival C.T. Ovoid/spindle shaped with branching processes; Pale staining elongated/disc like nucleus with basophilic cytoplasm Well developed RER, Mitochondria and Golgi complex. Fibrocytes- Produce ECM components of developing CT. Classified as: Lamellar / pyriform shaped – immature cells Spindle/ fusiform – intermediate cells Stellate/ star shaped – mature cells Fibroblast:

46. Functions: To secrete collagen and elastin, glycoproteins and GAG’s. Secrete active collagenase & MMP’s . Secrete number of growth factors, cytokines and inflammatory mediators like IL-1, IL-6, IL-8, TNF- α , PDGF, keratinocyte growth factor etc. Role in developmental processes, wound healing and tissue re-modelling. In health : produce & maintain ECM, role in homeostasis and modification of parts of matrix they created. In disease : enlarged, cytopathically altered due to dispersion of chromatin, formation of surface blebs, enlargement and dilation of mitochondria, breaks in plasma membrane.

47. MACROPHAGES: Derived from monocytes. Also known as tissue histiocytes. Spindle/irregularly shaped with oval nuclei. Short projections - phagocytosis. There are tissue macrophages and wandering macrophages.

48. Functions: In health: less well defined. Role in homeostasis. In disease: produce powerful hydrolytic enzymes: act as scavengers dispensing with the bacteria, toxins & debris. Release neutrophil chemotactic factors, PG’s , IL-1 that regulate immune response. Activated macrophages can regulate C.T turnover (potent substances – stimulate fibroblast proliferation – enhanced collagen production).

49. Neutrophils: Represent the first line of host defence mechanism. Omnipresent in gingival tissues and likely to play major role in periodontal homeostasis in health. Migrate rapidly from blood to enter the C.T as a result of immune response and tissue injury. Function: Play a role in phagocytosis by release of certain intracellular enzymes like myeloperoxidase, lysozyme, lactoferrin, collagenase-2 or PMN type collagenase or MMP-8 and alkaline phosphatase.

50. Ground substance: Proteoglycans: In gingiva: Decorin , biglycan , versican and syndecan . Bind growth factors, cytokines and other biologically active molecules. GAG’s in supra-alveolar fiber apparatus, loose connective tissue and basement membranes. glycoproteins Major - fibronectin, laminin, tenascin , elastin. Fibronectin: binds fibroblasts to fibres ; mediate cell adhesion and migration Laminins: attach basal lamina to epithelium.

51. Gingival fibres : Collagen fibres Elastic fibres – Oxytalin , elastin, elaunin Reticular fibres Functions: To brace the marginal gingiva firmly against the tooth. To provide the rigidity necessary to withstand the forces of mastication without being deflected away from the tooth surface. To unite the free marginal gingiva with the cementum of the root and the adjacent attached gingiva.

52. Three groups of fibers: Gingivodental group On the facial, lingual and interproximal surface embedded in the cementum just beneath the epithelium at the base of the gingival sulcus. They extend externally to the periosteum of the facial and lingual alveolar bones and terminate in the attached gingiva or blend with the periosteum of the bone. Circular group Course through the connective tissue of the marginal and interdental gingiva and encircle the tooth in ring like fashion. Transseptal group Form horizontal bundles that extend between the cementum of approximating teeth into which they are embedded.

53. According to Bartold : Primary fibers: Circular Dentogingival Dentoperiosteal Alveologingival Transseptal Secondary fibres : Periosteo -gingival Interpapillary group Inter gingival Transgingival Inter circular Semi circular Page and co workers: Semicircular and Transgingival

54. Clinical importance of gingival fibres : Circumferential supracrestal fiberotomy ( pericision ) Gingivoplasty of thick interdental papilla frenectomies

55. Epithelial connective tissue interface: The boundary between the oral epithelium OE and the underlying (CT) has a wavy course. The connective tissue portions which project into the epithelium are called connective tissue papillae (CTP) and are separated from each other by epithelial ridges — so-called rete pegs (ER). In normal gingiva, a characteristic morphologic feature of the oral epithelium and the oral sulcular epithelium is the presence of rete pegs, while these structures are lacking in the junctional epithelium .

56. Blood supply of gingiva: Three sources of blood supply to the gingiva are as follows Supraperiosteal arterioles   Vessels of periodontal ligament , which extend into the gingiva and anastomose with capillaries in the sulcus area. Arterioles which emerge from the crest of the interdental septa  

57. Vasculature: Nuki and Hock (1974) studied the organization of the gingival vasculature noting that the subepithelial vasculature consisted of a series of interconnecting capillary units made up of at least 2 terminal arterial capillaries, 4 primary venular capillaries, and numerous connecting vessels. The capillary units were among the first vessels affected by inflammation as evidenced by an increase in vessel width (5 to 10 \\m) and length (400 to 1,000 ^ im as well as alteration of vessel morphology

58. Lymphatics and nerve supply: Lymphatic drainage Lymphatics beneath the junctional epithelium extend into the periodontal ligament and accompany the blood vessels.   Gingival innervation It is derived from fibers arising from nerves in the periodontal ligament and from the labial buccal and palatal nerves The following nerve structures are present in the connective tissue, a meshwork of terminal argyrophilic fibers some of which extend into the epithelium. Meissner type- tactile corpuscles Krause-type end bulbs- temperature receptors Encapsulated spindles

59. Epithelial changes in disease: Epithelial permeability increases. The intercellular spaces of the J/E widen and serve as a primary pathway for the progress of the inflammatory exudate from the gingiva to the gingival sulcus . There is a significant influx of neutrophils that the intercellular spaces of the junctional epithelium become pathologically altered, with disruption to the intercellular junctions and increasing widening of the intercellular spaces.

60. Once this level of infiltration has occurred, and if the driving stimulus (dental plaque) remains, then the normal rapid turnover of the junctional epithelium is insufficient to restore health and the pathway to ongoing tissue damage is established. With continuing plaque accrual, neutrophil migration and early activation of macrophages and lymphocytes within the gingival connective tissue, the junctional epithelium can be seen to commence migration in an apical direction and result in the earliest formation of a periodontal pocket. Communicative pathways may be established through a variety of cells known to reside in the epithelium. For example, Langerhans cells, which act as antigen-presenting cells, have been noted to increase in number with increasing inflammation.

61. Connective tissue changes: Subsequent to the initial inflammatory response, CT destruction occurs within 3-4 days after plaque accumulation and begins at perivascular collagen bundles. As the inflammatory process continues, destruction expand deeper towards pdl and alveolar bone – tooth mobility. Simultaneously with destruction, fibrosis and scarring may coexist. Qualitative and quantitative changes occur to the gingival collagens, gingival proteoglycans . The glomerular nature of gingival plexus increases with increase in the number and size of the capillary loops. During this process, the post capillary venules adopt the appearance of high endothelial venules which facilitates emigration of lymphocytes.

62. Gingival biotypes: Pioneers: Ochsenbein and Ross

63. THICK Most prevalent. Consists of flat soft tissue. Thick bony architecture. Dense & fibrotic with large zone of attachment. More resistant to recession THIN Delicate Highly scalloped soft tissue. Thin bony architecture. Characterized by fenestration and dehiscence. More prone to recession, bleeding and inflammation

64. Methods to determine gingival biotype: Conventional histology on cadaver jaws Endodontic reamers Trans-gingival probing Histologic sections Cephalometric radiographs CBCT

65. Correlation of clinical and microscopic features: Colour Health Normally coral pink in color. Depends on the thickness and degree of the keratinisation of the epithelium and the presence of pigment producing cells. Alveolar mucosa is red, smooth and shiny. Epithelium is thinner, non keratinised and contains no rete pegs.

66. Physiological pigmentation: Melanin pigmentation – can occur as early as 3hrs after birth and often is the only evidence of pigmentation. According to Dummett: In Blacks Gingiva : 60% Hard palate : 61% Mucous membrane : 22% Tongue : 15%

67. Gingivitis:

68. Smokers melanosis melanoma Puetz juegher syndrome Hypermelanosis

69. LEAD TOXICITY COPPER PIGMENTATION MINOCYCLINE PIGMENTATION AMALGAM TATOO HEAVY METAL POISONING

70. SIZE: Health The size of the gingiva corresponds with the sum total of the bulk of cellular & intercellular elements & their vascular supply. Disease Size of the gingiva is enlarged and is called as gingival enlargement. Inflammatory- increase in cells and decrease in fibres. Non-inflammatory - decrease in cells and increase in fibres.

71. consistency Health The gingiva is firm and resilient with exception of the movable free margin. The collagenous nature of the lamina propria and its contiguity with the mucoperiosteum of the alveolar bone determines the firmness of the attached gingival margin. The normal consistency of the gingiva can be checked by palpation either with a blunt instrument or digital pressure. Disease: Pitting on pressure indicates soft and oedematous gingiva.

72. Shape: Anteriors :Triangular to knife-edged Posteriors : broader and more square shaped Factors affecting shape: Contour of proximal teeth. Location and shape of embrasure. In disease:

73. Contour: Facial & lingual surfaces: Scalloped Teeth with relatively flat surfaces: straight line Pronounced MD convexity, labially placed teeth: accentuated Linguo-version teeth: horizontal and thickened. Depends on Shape of teeth and their alignment in arch Location and size of area of proximal contact Dimensions of facial and lingual gingival embrasures

74. In disease: Thickened shelf like contour of gingiva on tooth in lingual version aggravated by local irritation caused by plaque accumulation. ACCENTUATED CONTOUR STILLMAN’S CLEFTS

75. In disease: Chronic gingivitis- marginal gingiva becomes rolled or rounded and interdental papilla becomes blunt and flat. ANUG - Punched-out crater like depressions at the crest of interdental papilla. Chronic desquamative gingivitis- irregularly-shaped denuded appearance of the gingiva. Gingival recession- exaggerated scalloping of the gingiva. Stillmans clefts : apostrophe shaped indentation extending from the gingival margin. Mc calls festoons : life-saver like enlargement on the marginal gingiva, most commonly seen on the canine and premolar facial surface.

76. Surface texture Health : The gingiva presents a textured surface similar to an orange peel and is referred to as being stippled. Best viewed by drying the gingiva. Attached gingiva is stippled but not marginal gingiva. Stippling is absent in infancy, appears in some children at about 5years age, increases until adulthood and frequently begins to disappear in old age. Form of adaptive specialisation or reinforcement for function

77. In Chronic inflammation Smooth and shiny gingival surface firm and nodular Smooth surface texture is also produced by epithelial atrophy in atrophic gingivitis and peeling of the surface occurs in Chronic desquamative gingivitis . Hyperkeratosis -leathery texture Drug induced gingival overgrowth- nodular surface.

78. Position: The normal position of the gingiva is 1mm above the cemento enamel junction. Physiologic factors Position of the teeth in the arch. Root-bone angle Mesio -distal curvature of tooth surface. Pathologic factors Toothbrush trauma. Gingival inflammation. High frenal attacment . Tooth malposition. Friction from soft tissue.

79. Traumatic lesions Physical injuries Chemical injuries Thermal injuries. In acute cases, the appearance of the slough (necrotising epithelium), erosion or ulceration and the accompanying erythema are the common features. In chronic cases, permanent gingival defects are usually present in the form of gingival recession

80. Continuous tooth eruption Eruption does not cease when teeth meet their functional antagonists but continues throughout life. Active tooth eruption is the movement of the teeth in the direction of the Occlusal plane, whereas passive tooth eruption is the exposure of the tooth by apical migration of the gingiva. This concept distinguishes between the anatomic crown and between the clinical crown and clinical root . Gottlieb and Orban believed that active and passive eruption proceed together. Originally, passive eruption was thought to be a physiological process. Now, it is considered as a pathologic process.

81. Effect of aging: On Gingival Epithelium Thinning & decreased keratinization. Flattening of rete pegs & altered cell density. Width of the AG increases. Gingival connective tissue coarser & more dense gingival CT. changes in collagen : -increased rate of conversion of soluble to insoluble collagen. -increased mechanical strength. -increased denaturing temperature.

82. Oxygen consumption of gingiva:

83. Conclusion: Knowing the normal gingival architecture in health is important to differentiate between health and disease state of an individual. Hence it is significant to understand the morphological and clinical alterations in the gingiva during disease state which helps us to identify the intensity and prognosis of a particular disease.

84. References: Newman,Takei,Klokkevold,Carranza.Clinical Periodontlogy.9 th edition, Elsevier pub,2002. Newman,Takei,Klokkevold,Carranza.Clinical periodontology 10 th edition, Elsevier publication,2002. Lang NP, Lindhe J. Clinical Periodontology and implant dentistry.5 th edition.Blackwell Munksgard:Oxford:2008 Nanci A , Bosshardt D. Structure of periodontal tissues in health and disease. Periodontol 2000 2006;40:11–28. I Glickman, Manhold , John H. The Oxygen Consumption of Healing Gingiva J DENT RES August 1950 29: 429-435. Mundeja N, Baiju CS, Khashu H, Jain D, Gupta A. Gingival biotype: A key determinant in periodontal treatment. Int J Dent Health Sci 2014; 1(4);552-565 Esfahrood ZR, Kadkhodazadeh M, Talebi Ardakani MR. Gingival biotype: a review. Gen Dent. 2013 Jul;61(4):14-7. Shah R, Sowmya NK, Thomas R, Mehta DS. Periodontal biotype: Basics and clinical considerations. J Interdiscip Dentistry 2016;6:44-9.