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Pdl and its clinical considerations (2)
- 1. GOOD AFTERNOON TEACHERSAND COLLEAGUES ! LIFE IS SHORT ,SMILE WHILE U STILL HAVE NATURAL TEETH ! 1
- 2. PDLAND ITS CLINICAL CONSIDERATIONS PRESENTED BY- DR.NANDINI BHARDWAJ DEPARTMENT OF ORAL PATHOLOGY , MICROBIOLOGY & FORENSIC ODONTOLOGY 2
- 3. CONTENTS INTRODUCTION DEVELOPMENT PERIODONTAL LIGAMENT HOMEOSTASIS CELL BIOLOGYOF NORMAL PERIODONTIUM CELLS EXTRACELLUALR SUBSTANCE STRUCTURES PRESENT IN CONNECTIVE TISSUE FUNCTIONS AGE CHANGES IN PERIODONTAL LIGAMENT CLINICAL CONSIDERATIONS SHOCK ABSORPTION THEORY REFERENCING 3
- 5. INTRODUCTION The periodontium isa connective tissue organ, comprising of CEMENTUM, PERIODONTAL LIGAMENT , BONE LINING THE TOOTH SOCKET ( ALVEOLAR BONE )& Part of gingiva facing the tooth ( dentogingival junction) The periodontium is attached to the dentin of the root by CEMENTUM & to the bone of jaws by ALVEOLAR BONE 5
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- 8. “The periodontal ligament iscomposed of complex vascular and highly cellular connective tissue that surrounds the tooth root & connects it to the inner wall of alveolar bone.” It is continuous with the connective tissue of the gingiva & communicates with the marrow spaces through vascular channels in the bone The periodontal ligament occupies the periodontal space. Between the cementum and periodontal surface of alveolar bone. Width ranges from 0.15 to 0.38 mm Thinnest around the middle third of the root with hour glass appearance.
- 10. The periodontal ligamentis a fibrous connective tissue ,that is cellular & contains numerous blood vessels. Comprises of Cells extracellular matrix ( fibers & ground substance) Collagen macromolecules ( proteins& polysaccharides) SYNONYMS •DESMODONT •PERICEMENTUM •DENTAL PERIOSTIU M •ALVEOLODENTAL LIGAMENT •PERIODONTAL MEMBRANE •PERIODONTAL LIGAMENT
- 11. . Hertwig ‘s epithelialroot sheath – epithelial cells grows apically Formation of cervical loop of tooth bud –continues proliferation of inner & outer enamel epithelium Root formation ,prior to tooth eruption DEVELOPMENT
- 12. As a result, they actively synthesize & deposit –collagen fibrils & glycoprotein's Perifollicular area gains polarity , cellular volume & synthetic activity. Dental follicle composed of -mesenchymal cells of dental follicle proper &perifollicular mesenchyme Developing & mature PDL – undifferentiated stem cells , potential to differentiate into osteoblasts , cementoblasts & fibroblasts.
- 14. Active fibroblasts adjacent tocementum of coronal third of root align in an OBLIQUE direction First collagen fiber bundles –discernible . Precursors of ALVEOLAR CREST fiber bundle group Upon tooth eruption – only ALVEOLAR CREST fibers are discernible HISTOLOGICALLY OBLIQUE FIBRES in the middle third of the root still in progress. As eruption continues & definite occlusion established- apical maturation of oblique fiber bundles & definite PDL architecture HORIZONTAL FIBRES almost developed during first occlusal contact of the tooth with its antagonist DEVELOPMENT OF PRINCIPAL FIBRES
- 17. DENTAL FOLLICLE PROPERcells- aligned parallel •Disruption of root sheath- dental follicle proper cells assume an elongated profile . •Polarity towards dentin matrix . •Collagen bundles- reorganized •Oriented perpendicular to the root surface PDL collagen fiber attachment to the root surface
- 18. •Maintains its width( matrix gla protein) •Inhibits mineralized bone nodule formation •MsX2( homeobox protein ) prevents osteogenic differentiation of PDL fibroblasts •Unminerlised PDL – bone sialoprotein ,osteopontin & glycosaminoglycans. PDL HOMEOSTASIS -Maintaining the unmineralised PDL
- 20. GROWTH FACTORS • Fibroblastgrowth factor. • Interleukin -1 ( IL-1) • Platelet derived growth factor ( PDGF) • Transforming growth factor ( TGF) • Interferon gamma • Matrix metalloproteinase's & their tissue inhibitors (MMP’s) CYTOKINES CELL BIOLOGY OF NORMAL PERIODONTIUM
- 21. FIBROBLAST GROWTH FACTOR(FGF) •Acidic FGF – DNA synthesis , cell replication – INCREASE PROTEIN SYNTHESIS ( type 1 collagen ). •Basic FGF – Antigenic property,chemotactic & mitogenic , cell replication . •Potent stimulator of periodontal cell migration & mitogenesis.
- 22. INTERLEUKIN -1 (IL-1) •Immunity,inflammation, tissue breakdown ,tissue homeostasis. •KEY ROLE – pathogenesis of bone diseases & adult periodontitis. •Synthesize – type 1 procollgen,collagenase ,hyaluronic acid,fibronectin & PGE2 •Stimulates bone resorption.
- 23. PLATELET DERIVED GROWTH FACTOR(PDGF) •Consists –A & B disulphide bonded polypeptide chains. •INCREASES cell proliferation, but also increases bone resorption (prostaglandin synthesis).
- 24. TRANSFORMING GROWTH FACTOR (TGF) •Polypeptideisolated from normal & neoplastic tissues •CAUSE- change in normal cell growth
- 25. INTERFERON GAMMA •Immunomodulatory effects •Thus, is a LYMPHOKINE AS MUCH AS AN INTERFERON •Affects – collagen production ( turn of collagen gene expression)
- 26. MATRIX METALLOPROTEINASES ( MMP’s) •Works – neutral Ph •Digest – all major matrix molecules . •TGF beta – repress MMP production .
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- 29. FIBROBLASTS •Most prominent cellsin PDL •LONG AXIS - parallel to the direction of collagen fibrils. •PRODUCES- structural connective tissue proteins, collagen , elastin , glycoprotein's & glycosaminoglycans •Secretes – collagenases & MMP’s •RESPONSIBLE - formation & remodeling of PDL fibers •SIGNALING SYSTEM to maintain width & thickness of PDL
- 31. CEMENTOBLASTS •LOCATION – adjacentto cementum •Cells actively depositing cellular cementum – abundant basophilic cytoplasm & cytoplasmic processes •Cells depositing acellular cementum – no prominent cytoplasmic processes
- 33. OSTEOBLASTS • Bone formingcells •Cuboidal , prominent round nucleus •ABUNDANT – rough endoplasmic reticulum , mitochondria & vesicles •Cell appear basophilic due to the presence of abundant RER. •Microfilaments – Prominent •CELL CONTACT- desmosomes, cytoplasmic processes & tight junctions.
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- 36. FIBROBLASTS •Rapid degeneration ofcollagen by fibroblast phagocytosis. •PHAGOCYTOSIS- basis for last turnover of collagen in PDL
- 38. CEMENTOCLASTS •Resemble osteoclasts • occasionallyfound in normal PDL
- 39. OSTEOCLASTS •Resorbing cells •Large &multinucleated ( can be mononuclear ) •Occupy Howship’s lacunae or surround the end of bone spicule
- 41. •Described by malassezin 1884 •Remnants – Hertwig’s epithelial root sheath. •LOCATION – furcation areas •FUNCTION – not clear , periodontal repair & regeneration •( ORBAN’S oral histology & embryology )
- 44. •Undergo mitotic division •Location-adjacent to blood vessels. •Stem cell features- small size ,responsiveness, slow cycle time •Small closed faced nucleus , very little cytoplasm CELLS
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- 47. MAST CELLS •Small ,round or oval •Associated with blood cells. •Histamine – role in inflammatory reaction •Occasional mast cells seen in – Healthy PDL
- 50. MACROPHAGES •Phagocytosis •Secretes growth factors •Synthesizeinterferons & prostaglandins
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- 55. FIBRES • Collagen • Elastic •Reticular • Secondary • Indifferent fiber plexus Oxytalan GROUND SUBSTANCE • Proteoglycans • Glycoprotein's EXTRACELLULAR SUBSTANCE
- 56. ALVEODENTAL LIGAMENT • Alveolar crestgroup • Horizontal group • Oblique group • Apical group • Interradicular group PRINCIPAL FIBRE GROUP
- 57. ALVEOLAR CREST GROUP EXTENSION–obliquely from cementum beneath the junctional epithelium to the alveolar crest . FUNCTION – resist tilting , intrusive , extrusive & rotational forces
- 59. HORIZONTAL GROUP •Run atright angle to the long axis of tooth from cementum to the bone. •Roughly parallel to the occlusal plane LOCATION – immediately apical to the alveolar crest fibers. FUNCTION – resist horizontal & tipping forces
- 61. OBLIQUE GROUP •Most numerous •Occupynearly 2/3rd of the ligament. FUNCTION- resist vertical & intrusive forces
- 63. APICAL GROUP •Anchored intothe fundus of bony socket. • Not seen on incompletely formed root •FUNCTION- Resist forces of luxation , tipping ,protect blood , lymph & nerve vessels.
- 65. INTERRADICULAR GROUP •Crest ofinterradicular septum in multirooted teeth. • FUNCTION – resist tooth tipping , torquing & luxation •Partial loss – gingival recession. •Total loss – chronic inflammatory periodontal disease.
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- 68. •Gathered to formbundles •Submits in bundles –COLLAGEN FIBRILS •Main type of collagen in PDL – type 1 & type 3 •Type I – uniformly distributed •Type 3 – 20 % of collagen fibrils , covalently linked to type 1 collagen throughout the tissue •Small amount – type 5 & type 6 collagen •Traces –type 4 & type 7 COLLAGEN
- 70. SHARPEY’S FIBRES •DEFINITION –Collagenfibers are embedded into cementum on one side of the periodontal space & into the alveolar bone on the other. The embedded fibers are termed as sharpey’s fibers. •FUNCTION –attaches muscle to periosteum.
- 73. ELASTINFIBERS LOCATION – afferent bloodvessels. Microfibrillar component-ELASTIN PROTEIN CONTENTS –glycine, proline , hydrophobic residues( hydroxyproline) ELAUNINFIBERS Bundles of micro fibrils embedded in amorphous –ELASTIN PROTEIN. OXYTALANFIBERS DIRECTION- Axial FUNCTION – Unknown , may play a part in supporting the blood vessels of PDL ELASTIC FIBRES
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- 77. PROTEOGLYCANS Two proteoglycans inPDL – •Proteodermatan sulfate •Proteoglycan containing chondroitin sulfate /dermatan sulfate hybrids(PG1)
- 79. GLYCOSAMINOGLYCANS Linear polymers ofdisaccharide. consists of hexosamine, heparin sulfate & hexuronic acid OTHER COMPONENTS Substrate adhesion molecules – tenacsin, osteonectin, laminin, undulin & fibronectin
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- 83. BLOOD VESSELS •ARTERIAL SUPPLY– •Branches from apical vessels that supply the dental pulp. •Branches from intra-alveolar vessels •Braches from gingival vessels.
- 85. LYMPHATIC DRAINAGE The flowis from ligament towards and into the adjacent alveolar bone.
- 86. CEMENTICLES •Calcified bodies • •Spheroidal orovoid •Embedded to the cementum or lying free within PDL
- 88. NERVE SUPPLY •SENSORY •Branches ofmaxillary & mandibular division of fifth cranial nerve (mechanoception) •AUTONOMIC •PDL vessels
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- 91. •Suspensory ligament • Toothsupport – collagen fibers, vasculature & ground substance SUPPORTIVE
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- 95. SENSORY •Mechanoreception •ACTING BINDING PROTEIN– 280 • reinforce membrane cortex •Increase strength of cytoskeleton links to the extracellular matrix •Desensitizing stretch activated ion channel activity
- 96. NURTITIVE •Anabolies & othersubstances •Major anastomosis between blood vessels in the adjacent marrow spaces & gingiva
- 97. HOMEOSTATIC •Insight into thebiological mechanisms
- 98. ERUPTIVE •Provides space • Mediumfor cellular remodeling
- 99. PHYSICAL •Protection of vessels& nerves from mechanical forces •Resistance to impact from occlusal forces.
- 100. AGE CHANGES INPDL •Cell number & cell activity- DECREASES •Vascularity – DECREASES •PDL width start to dwindle
- 101. UNIQUE FEATURES OFPDL •CELLS THAT FORM & RESORB CEMENTUM & BONE & the collagen fibers in specific orientation connecting the two mineralized tissues making it unique •EXTREMLY CELLULAR with fibroblasts well innervated with mechanoreceptors & highly vascular unlike any other connective tissue in adult. •PDL bears a resemblance to immature , fetal like connective tissue s •The features being , high cellularity ,high rates of turnover & significant amount of type III Collagen . •The ground substance occupies large volume of proteoglycans & glycoproteins . •Thus the PDL has structural , ultrastructural &biochemical features like fetal tissue
- 102. Clinical considerations The primaryrole of periodontal ligament is to support the tooth in the bony socket . Its thickness varies in different individuals , in different teeth in the same person & different locations on the same tooth . Measurements of large number of ligaments range from 0.15- 0.38 mm. Fulcrum of physiological movement seen in the middle region of root as the PDL is thinnest in this region . Thickness of the PDL is maintained by the functional movements of the tooth .Thin in functionless & Embedded tooth & wide in teeth under excessive occlusal stresses To carry the load suddenly placed on the tooth by restoration, the supporting tissues of tooth are poorly adapted. Also in bridge abutments , teeth opposing bridges or dentures, teeth used as anchorage for removable bridges. Resulting in inability of the patient to use a restoration immediately after the placement
- 104. Acute trauma tothe PDL , accidental blows ,rapid mechanical separation produce pathologic changes such as fractures or resorption of the cementum ,tear of fiber bundles, hemorrhage & necrosis . Adjacent alveolar bone is resorbed ,PDL widened & the tooth becomes loose .when trauma is eliminated repair usually takes place Orthodontic tooth movement depends on tooth resoption & formation of both bone & periodontal ligament stimulated by regulated pressure & tension . The stimuli are transmitted through the periodontal ligament . If the movement of the teeth is within physiological limits , the initial compression of PDL on the pressure side is compensated for by bone resorption , whereas on the tension side bone apposition is seen . Application of large forces results in necrosis of periodontal ligament & alveolar bone on the pressure side & the movement of tooth will occur only after the necrotic bone is resorbed by osteoclasts located on the endosteal surface.
- 105. The periodontal ligamentin the periapical area is often the site of pathologic lesion .Inflammatory diseases of the pulp progress to the apical periodontal ligament & replace its fiber bundles to the granulation tissue . This lesion called periapical granuloma , may contain periapical cells which undergoes proliferation & produces a cyst . The periapical granuloma & the periapical cyst are the most commonest pathologies of the jaws . Last but not the least , the commonest pathology related to PDL is chronic inflammatory periodontal disease . The toxins released from the bacteria in the dental plaque & metabolites of the host defense metabolism destroys the PDL & Adjacent bone very frequently . Periodontal disease results because of periodontal bacteria coupled with specific host inflammatory response . Progression of periodontal disease results in tooth mobility & further loss of tooth . Limiting the disease process requires regeneration of host tissues of PDL & BONE so that reattachment of the PDL to the bone becomes possible .
- 106. Correction of PDLdestruction – guided tissue regeneration Implantation of surgical substituted have included – tube of auto grafts ( cortical , cancellous bone , bone marrow ) Auto grafts ( deminerlised freeze dried /freeze dried bone ) & alloplastic materials like ceramic ,hydroxypatite , polymers & bioglass Recently tissue engineering principles + biological principles like gene therapy , use of biocompatible scaffolds are being used . Bioactive molecules such as growth factors , cytokines , bone morphogenic protein , enamel proteins ( amelogenin /enamel matrix protein ) , natural bone mineral induce periodontal cells & help in periodontal regeneration . The use of progenitor cells /mesenchymal stem cells to regenerate PDL comes as newer option towards tissue repair & regeneration .