1. ISTOLOGY Ma. Concepcion B. Medina, DDM. Oral Medicine Section College of Dentistry, University of the Philippines Manila Taft Avenue corner Pedro Gil St., Ermita, Manila H I NFLAMMATION

2. Features of the Pulp Low compliance environment Nature of its blood supply High pulpal tissue fluid pressure Fluid in tubules - Effect on DF flow? Protective mechanisms

3. Protective Response of Pulp to Caries 1. Decrease in permeability Kim, et.al., 2002

4. Sclerosis Caries  dentin is demineralized  Precipitation of minerals Stimulation of odontoblasts Sclerosis

5. Protective Response of Pulp to Caries 1. Decrease in permeability 2. Tertiary dentin formation Kim, et.al., 2002

6. Tertiary dentin

7. Protective Response of Pulp to Caries 1. Decrease in permeability 2. Tertiary dentin formation Where formed? Which histologic feature of the pulp is involved? Mechanism?

8. Caries  dentin is demineralized  dentin proteins released  Cytokine expression by pulp cells (odontoblasts, fibroblasts, dendritic cells) – IL-8 for PMNs; those that induce vascular permeability, promote dentinogenesis & repair, arrest caries progression (TNF, GFs) Barkhorder, et.al, 1999; Tyler, et.al., 1999; Lim, et.al, 1994

9. Protective Response of Pulp to Caries 1. Decrease in permeability 2. Tertiary dentin formation 3. Inflammatory and adaptive immune reactions Kim, et.al., 2002

10. Innate immune response Adaptive immune response Immune Response Macrophages PMNs Lymphocytes First line of defense Initiates adaptive response

11. Injury: bacteria by products Odontoblasts  Afferent nerves  Cells  INFLAMMATION cytokines neuropeptides mediators of inflammation

12. Vascular, cellular, neurogenic response to injury Acute phase – “exudative” Chronic phase – “proliferative” Protective reaction, BUT … Inflammation

13. Vascular changes Injury  VC  VD  Plasma extravasation Blood volume P CAPILLARIES Permeability redness heat

14. Vascular changes Plasma extravasation Swelling PTPT ReversibleP nerves

15. localized inflammation (reversible) remove cause healing

16. Countermeasures vs increase in P T Increased absorption by capillaries in adjacent uninflamed areas Increased lymphatic drainage No further filtration from capillaries REMOVE CAUSE  HEALING

17. Vascular changes Plasma extravasation Swelling PTPT P BV > Blood flow Reversible

18. Vascular changes Blood flow P02P02 P CO 2 pH Necrosis Pus formation = microabscess

19. microabscess inflammation Irreversible Necrosed inflammation “Injury”

20. Vascular changes Blood flow P02P02 P CO 2 pH Necrosis Pus formation = microabscess

21. Cellular changes Blood flow WBCs (PMNs) Margination Emigration Phagocytosis Pavementing Aggregation Proteolytic enzymes Microabscess

22. Injury: bacteria by products Odontoblasts  Afferent nerves  Cells  INFLAMMATION chemokines neuropeptides mediators of inflammation neuropeptides

23. Neurogenic changes Neuropeptides (sensory nerves) CGRP, SP, VIP, Neuropeptide Y, Neurokinin A Cause VD, inc. vascular permeability, pain modulation Regulate chemokine production by pulp cells Promote wound healing

24. Injury: bacteria by products Odontoblasts  Afferent nerves  Cells  INFLAMMATION chemokines neuropeptides mediators of inflammation

25. Mediators of inflammation Histamine  VD; inc. vascular permeability Cytokines  Kinins  pain

26. Periradicular Lesions Bacteria &/or by products apical foramen Inflammation : Neuropeptides Chemokines Inflammatory mediators Chemokines Macrophages PMNs Lymphocytes Macrophages Osteoclasts Fibroblasts

27. Other likely inducers of chemokine production in PLs: Periradicular Lesions Trauma Injury from instrumentation Irritation from endo materials Silva, et.al., 2007

28. Injury  VC  VD  Plasma extravasation Blood volume P CAPILLARIES Permeability redness heat Periradicular Lesions

29. Plasma extravasation Periradicular Lesions Inflammatory exudate Intraperiapical pressure (+) percussion

30. Plasma extravasation Swelling PTPT P BV > Blood flow Periradicular Lesions

31. Blood flow P02P02 P CO 2 pH Necrosis Pus formation Periradicular Lesions (+) palpation

32. Chronic state Lymphocytes Plasma cells Fibroblasts Collagen synthesis + new blood vessels = GRANULATION TISSUE Adaptive IR

33. Chronic state Granuloma Cyst

34. Localized abscess formation (grinding of rat molars) 12-24 hrs.  phagocytosis 48 hrs.  collagen synthesis by newly differentiated odontoblasts Sveen, 1972

35. Localized abscess formation (grinding of rat molars) 3-8 days  mineralization  3 o D or scar tissue formation The inflammation that resulted from the inflicted trauma resolved. Sveen, 1972

36. Localized abscess formation (humans) 19 days post-injury  differentiation of odontoblast- like cells 100 days  reparative dentin barrier 0.12 mm. thick

37. Clinical implications Healing may take place as a result of timely intervention. (pre-injury status of pulp) Minimize trauma to provide the best possible opportunities for future pulpal healing. Heyeraas, et.al, 2001

38. Clinical implications Healing may take place as a result of timely intervention. Healing may be in the form of 3 o D or scar tissue formation  Heyeraas, et.al, 2001 volume  reparative ability

39. Clinical implications Minimize trauma Effective water cooling system Light, intermittent pressure Avoid prolonged air drying

40. Summary Inflammation is a protective response. Healing will take place if the cause is removed (ie., the cavity is cleaned and restored).

41. Summary It is the clinician’s duty to minimize trauma to the pulp during restorative procedures. The principal threat to pulp health is caries. Ingle, et.al., 2008 The 2 nd most significant threat is the treatment of caries. Ingle, et.al., 2008

42. Cohen S and Burns R: Pathways of the Pulp 8 th ed., 2002. Walton R and Torabinejad M: Principles and Practice of Endodontics, 2002 and 2009. References Cohen and Hargreaves: Pathways of the Pulp 9 th ed., 2006.

43. Janeway C and Travers P: Immunobiology 3 rd ed., 1997. References Ingle, et.al.: Ingle’s Endodontics 6 2008.

44. Part 1. Normal structure and physiology. #6 pp. 427-446 Part 2. Initial reactions to preparation of teeth for restorative procedures. #7 pp. 537-551 Part 3. Pulpal inflammation and its sequelae. #8 pp. 611-625 Quintessence International 2001 Vol. 32: Pulp-dentin Biology in Restorative Dentistry

45. Chemokines in Oral Inflammatory Diseases: Apical Periodontitis and Periodontal Disease Silva, et.al. Journal of Dental Research 2007 Vol. 86, No. 4