1. Libyan International Medical University 2nd Year First Semester D Caroline Piske de A. Mohamed

2. Objectives Learning issues and objectives: What is meant by periodontium? What are its various components? Describe the functions of periodontium and how they are performed.

7. PERIODONTIUM Cementum PDL Alveolar bone Sharpey's fibers Attachment organ Cementum Periodontal ligament Alveolar bone Apical foramen Pulp cavity Enamel Dentin Gingiva Root canal Alveolar vessels & nerves

10. FUNCTIONS OF PDL SUPPORT: PDL supports teeth in their socket. It prevents loosening of teeth. MASTICATORY LOAD: PDL permits teeth to withstand the considerable forces of mastication. SENSORY: PDL is supplied by abundant receptors and nerves that sense the movement when teeth are in function. Helps in the proper positioning of the jaws during normal function.

11. NUTRITIVE: Blood vessels of ligament provide essential nutrients for the ligament’s vitality and hard tissue of cementum and alveolar bone. Fibroblasts, osteoblasts, cementoblasts, and even resorptive osteoclasts and macrophages require nutrition.

12. CLINICAL CORRELATION: Bone, PDL, and the cementum together form a functional unit of special importance when the orthodontic tooth movement is undertaken. Orthodontic forces causes compression and constriction of blood vessels, soft tissue changes occur. Hence loss of alveolar bone occurs, now blood flow occurs in the spaces. And the mesenchymal cells of PDL repair the tissues.

13. MAINTAINENCE: Tissues are maintained under the influence of heavy masticatory forces. ADAPTIVE ROLE SHOCK ABSORBER: It absorbs the shock of chewing.

14. PRINCIPAL FIBER BUNDLES OF PDL 1. THE ALVEOLAR CREST GROUP These are attached to the cementum just below the cementoenamel junction and running downward and outward to insert into the rim of the alveolus.

15. 2.THE HORIZONTAL GROUP These are just apical to the alveolar crest fibers and running at right angles to the long axis of the tooth from the cementum to the bone below the alveolar crest.

16. 3. THE OBLIQUE GROUP They are the most numerous in the PDL and running from the cementum in an oblique direction to insert into the bone coronally

17. 4.THE APICAL GROUP: These are radiating from the cementum around the apex of the root to the bone forming the base of the socket.

18. 5.THE INTERADICULAR GROUP Found only in the multi-rooted teeth and running from the cementum into the bone forming the crest of the Interradicular septum.

19. TEETH IN-SITU

31. TYPES OF CEMENTUM CEMENTUM is classified according to the presence or absence of cells within its matrix. CELLULAR CEMENTUM, which has an adaptive role in response to tooth wear and movement and is associated with repair of periodontal disease. ACELLULAR CEMENTUM, which provides attachment for the tooth. A- CELLULAR CEMENTUM B-ACELLULAR CEMENTUM

49. Materia alba Bacterial aggregations, leucocytes and desquamated oral epithelial cells accumulating at the surface of plaque and teeth, but lacking the regular internal structure observed in dental plaque. ( mouth rinse can desegregate it) D Caroline Mohamed 49

51. Dental plaque Dental plaque is the soft, nonmineralized bacterial deposit which forms on teeth and dental protheses that are not adequately cleaned. LÖe 1965 Microscopically, plaque is simply confluent colonies of microorganisms connected by a matrix consisting predominantly of bacterial and salivary polymers. These accumulations subject the teeth and gingival tissues to high concentrations of bacterial metabolites, which result in dental disease. The dominant bacterial species in dental plaque are Streptococcus sanguis and Streptococcus mutans, both of which are considered responsible for plaque. D Caroline Mohamed51

52. Differences between materia alba, plaque and calculus D Caroline Mohamed 52

53. Major sites of plaque accumulation Fissures of molar teeth Supragingival: on the tooth surface above the gingiva Subgingival: in the area bounded by the margin of the gum and the tooth Interproximal: between adjacent teeth

54. Plaque formation

55. Plaque formation is initiated by a weak attachment of the streptococcal cells to salivary glycoproteins forming a pellicle on the surface of the teeth. Bacteria adhere to the pellicle, and pellicle coats the enamel. The specific type of bacteria/pellicle adherence is determined by the innate characteristic of the bacteria and the pellicle. Gram positive rods and cocci are laid down in the first hour. Time elapsed 1 hour

56. The initial bacteria are called pioneer colonizer, because they are hardy and successfully compete with other members of the oral flora for a place on the tooth surface.

57. Primary colonizers D Caroline Mohamed57 Generally the primary colonizers are not in sufficiet number to be pathogenic. Overwhelming cocci, specially streptococci and short rods.

58. Gram-positive facultatively anaerobic Streptococcus sanguis is most dominant first to appear followed later by S. Mutans. Actinomyces spp. are also found in 24h plaque. Gram-positive cocci and rods co-aggregate and multiply. 58D Caroline Mohamed

59. This is followed by a stronger attachment by means of extracellular sticky polymers of glucose (glucans) which are synthesized by the bacteria from dietary sugars (principally sucrose). An enzyme on the cell surface of Streptococcus mutans, glycosyl transferase, is involved in initial attachment of the bacterial cells to the tooth surface and in the conversion of sucrose to dextran polymers (glucans) which form plaque. Bacteria adhere, multiply and increase in mass and thickness and form mini – colonies in layers upon the pellicle (plaque formed by rod and cocci only). Time elapsed 24-48 hours D Caroline Mohamed59

60. Within a short time, the tooth surface adjacent to the gingiva is covered by intermeshed bacteria. New bacteria derived from saliva or surrounding mucous attach by a bonding interaction to bacteria already attached to the plaque. All this activity occurs within the first 2 days of plaque development and, for description purposes, is called phase I of plaque formation.

61. In phase II of plaque development, the outer surface of the plaque is covered by gram-positive tall rods. There is a dramatic increase in plaque thickness 3 and 4 days compared to the first two days.

62. Secondary colonizers 62D Caroline Mohamed Adhere to bacteria already in the plaque mass. Surface receptors on the Gram-positive facultative cocci and rods allow the subsequent adherence of Gram-negative organisms, which have a poor ability to directly adhere to the pellicle. Fn: Fusobacterium nucleatum. BI: Prevotella intermedia.

63. Any area where the plaque has not been removed, either because of no home care or ineffective techniques, the bacteria mass continues to grow with a more complicated mixture of bacteria ( fusobacteria and filamentous). As the plaque thickens at the cervical area, the deeper layers incorporate more filaments and fusiforms, eventually turning gram negative. The coronal plaque is a more simple early arrangement of rods and cocci. Time elaped 4-7 days D Caroline Mohamed63

64. Micro-colonies D Caroline Mohamed64

65. Microcolonies coalescing D Caroline Mohamed65

66. In phase III, 4 to 7 days after initiation, plaque begins to migrate subgingivally, and bacteria and their products permeate and circulate in the pocket. The heterogeneity increases as plaque ages and matures. As a result of ecologic changes, more Gram-negative strictly anaerobic bacteria (fusobacteria, veillonellae) colonize secondarily and contribute to an increased pathogenicity of the biofilm.

67. In phase IV, 7 to 11 days after initiation of plaque development, the diversity of the flora increases to comprise motile bacteria including spirochetes and vibrios as well as fusiforms and white blood cells appear. The plaque becomes more gram negative and anaerobic in the deeper layers, the gums become slightly inflamed. Time elapsed 7-14 days D Caroline Mohamed67

68. Vibrios and spiroquetes continue to multiply. The bacteria in the dental plaque become highly organized, filamentous, are perpendicular to the tooth surface, and pulsate in a palisade fashion. The signs of inflamed gums are obvious. Time elapsed 14-21 days D Caroline Mohamed68

69. The increasing thickness of the plaque limits the diffusion of oxigen to the entrapped original oxigen- tolerant populations, as a result the organisms that survive in the deeper parts of the plaque are either facultative or obligate anaerobes as fusobacteria and veillonese D Caroline Mohamed69

70. Filamentous bacteria D Caroline Mohamed70

71. “ corn-cob ” associations D Caroline Mohamed 71

72. This mature plaque is now so packed with diverse bacteria that an exogenous species would have great difficulty becoming established in the overcrowded habitat. With time, more bacteria migrate subgingivally, and the process continues more aggressively.

73. Clean substratum Molecular adsorption (Phase 1) Single organisms (Phase 2) Multiplication (Phase 3) Sequential adsorption of organisms (Phase 4) 73D Caroline Mohamed

74. Mature dental plaque D Caroline Mohamed74

75. Calculus Composition 1. inorganic content 70-90% of calcium phosphate, calcium carbonate, magnesium phosphate 2.organic content protein-polysaccharide, desquamated epithelial cells, leukocytes, microorganisms

76. Calculus formation Calculus is dental plaque that has undergone miniralization Soft plaque.......precipitation of miniral salts between 1 st and 14 days Saliva is the source of miniralization Gingival Cervicular Fluid (GCF)

77. Health Gingivitis Periodontitis

78. Normal dental plaque: coccis, filaments, epithelial cell, little motility Gingivitis plaque: spirochetes and great motility

79. The critical locus of activity is the subgingival space (periodontal pocket). The bacteria residing in the pocket and the host cells that defend it determine the clinical outcome. The diseased periodontal pocket harbors both attached subgingival plaque biofilms and nonattaching, motile subgingival microflora (spirochetes, vibrios, and straight rods with flagella).

80. Orland et al (1954) demonstrated germ-free animals do not develop caries. In humans, when bacteria are allowed to accumulate in plaque on the tooth surfaces, enamel caries and gingivitis develop within 2 or 3 weeks.

81. Periodontal Disease

82. How do we know there is a problem?? DIAGNOSIS Individual complaine Clinical examinations Radiographic examination

83. Individual complaine Bleeding gums Red gums Blood on my pilo Bad taste Bad smell (halitosis) Smokers....less bleeding

84. Clinical examinations Plaque index Gingival index Pocket measurment Furcation Tooth mobility

86. Plaque Scoring System for Quigley and Hein Score no plaque 0 flecks of stain at the gingival margin 1 definite line of plaque at the gingival margin 2 gingival third of surface 3 two thirds of surface 4 greater than two thirds of surface 5 Plaque Index total score = = SUM(scores for all faal and lingual surfaces) index = = (total score) / (number of surfaces examined)

88. Gingival Index Löe & Silness 1963 Score 0Score 2 Score 3Score 1

89. Gingival Index: GI 0 1 2 3

90. AppearanceBleedingInflammationPoints normalno bleedingnone0 slight change in color and mild edema with slight change in texture no bleedingmild1 redness, hypertrophy, edema and glazing bleeding on probing/pres sure moderate2 marked redness, hypertrophy, edema, ulceration spontaneous bleeding severe3 Gingival Index Löe & Silness 1963

91. Teeth examined: (1) maxillary right first molar (2) maxillary right lateral incisor (3) maxillary left first bicuspid (4) mandibular left first molar (5) mandibular left lateral incisor (6) mandibular right first bicuspid

92. Surfaces examined on each tooth: (1) buccal (2) lingual (3) mesial (4) distal Gingival Index Löe & Silness 1963

93. Average Gingival IndexInterpretation 2.1 - 3.0severe inflammation 1.1 - 2.0moderate inflammation 0.1 - 1.0mild inflammation < 0.1no inflammation Gingival Index Löe & Silness 1963

94. Sign the worse score Choose the worse score Sign the worse score