DENTAL PULP & PERIAPICAL TISSUES - PATHOLOGY. Adjunct Associate Professor Lim Kian Chong Faculty of Dentistry National University of Singapore

Transcription

1 DENTAL PULP & PERIAPICAL TISSUES - PATHOLOGY Adjunct Associate Professor Lim Kian Chong Faculty of Dentistry National University of Singapore

2 Scope Understand the causes of pulpal injury Understand how pulp disease develops and eventually causes periapical disease

3 Lecture Outline Causes of pulp injury Pulpal reaction to injury Pathogenesis of pulpal and periapical disease (Terminology used in the clinical diagnosis of pulp and periapical pathosis)

4 Introduction The dental pulp is a unique tissue Dental pulp is enclosed in a rigid mineralized structure Udo M. Spornitz, Institute of Anatomy, Basel

5 Introduction Low compliant system No collateral circulation

6 Pulpo-Dentine Complex Udo M. Spornitz, Institute of Anatomy, Basel 0.5µ : 8000/mm 2 2µ : 60000/mm 2 Dentine is permeable Permeability increases the less the remaining dentine thickness

7 Pulpo-Dentine Complex Dentine is permeable Permeability increases the less the remaining dentine thickness Pulp and dentine must be considered as a continuum : pulpodentine complex X 730

8 Causes of Pulp Injury

9 Pulp Injury Bacterial Caries Microleakage Periodontal disease Trauma Iatrogenic Tooth tissue removal Heat Chemical Orthodontics caries blood supply disruption crack or fracture microleakage Healthy pulp can tolerate +5.5 o C No water o C

10 Pulpal Response to Injury Type Example Pulp Reaction Outcome Short term Long term Cavity preparation, trauma without luxation Caries, erosion, attrition, breakdown of restoration Acute inflammation Chronic inflammation Healing and recovery (once stimulus is removed) Pulp necrosis Trauma Luxation, avulsion Necrosis Infection of pulp space if bacteria present Yu & Abbot (2007)

11 Iatrogenic Irreversible Pulp Injury Procedure RCT needed Study AR or CR 2.7% (estimate) Deep caries/exposure:or=7.8 CR vs AR:OR=3.92 Whitworth et al. (2005) Crowns 3% Goodacre et al. (2003)* Bridges 11% Goodacre et al. (2003)* Root planing 3% Bergenholtz & Nyman (1984) Orthodontics * Meta-analysis # Literature review Rare unless previously traumatized Hamilton & Gutmann (2001)#

12 Caries the starting point of pulpal pathosis

13 Caries: Polybacterial Infection Gram +ve organisms dominate Change in mix from facultative to obligate anaerobes as depth of invasion increases Gram -ve anaerobes less frequent

14 Pulpal Response to Enamel Caries Pulp is affected once integrity of its protective chamber is breached Enamel is permeable Brännström & Lind (1965)

15 Biofilm: Bacteria Teichoic Acid Glycolipid Lipoteichoic Acid (LTA) Gram Positive Gram Negative Polysaccharide Lipid A Lipopolysaccharide (LPS)

16 Pulpal Response to Enamel Caries Pulp is affected once integrity of its protective chamber is breached Brännström & Lind (1965)

17 Dentine Caries Two layers of carious dentine: Infected dentine (outer layer) Affected dentine (inner layer) destruction bacterial penetration remineralization sclerotic

18 Pulpal Response to Caries The Pulp at War

19 Pulpal Response to Caries Innate immune response Adaptive immune response Cell-mediated Humoral (specific antibody) >2mm <2mm Shallow to moderate caries Deep caries Hahn & Liewehr (2007)

20 Enemy bacteria Innate Immune Response encountered.. Organize our defences immediately..get reinforcements! MD2 LPS CD14 TLR4 TLR4 LPS NF-ƙB pathway LTA TLR6 TLR2 Anitimicrobial peptides Pro-inflammatory Cytokine transcription Anti-inflammatory Antimicrobial Inflammation Neurogenic Inflammation LTA Chemokines Cell Recruitment

21 Innate Immune Response caries Dentinal Fluid Outward flow of dentinal fluid with intratubular immunoglobulin mdc CCL2 CXCL12 CXCL14 BD-2 TGF-β idc, Mo Cytokine transcription induced VEGF Vascular permeability Tissue pressure IL8 Neutrophils CXCL 10 NK cells Macrophages NP Neurogenic Inflammation

22 Neurogenic Inflammation Increase pulpal tissue pressure Increase dentinal fluid outflow Tertiary & sclerotic dentine formation Caviedes-Bucheli (2008)

23 Summary: Innate Immune Response Odontoblasts initiates response Inflammation compartmentalized to pulp adjacent to caries Slows bacterial invasion dentinal fluid outflow dentine permeability Intratubular mineralization Tertiary dentine formation tertiary dentine sclerotic dentine

24 Caries: Reactionary Dentine 2μ 2μ Charadram et al. (2012) Normal dentine Reactionary dentine

25 Innate Immune Response Dilutes toxins Cannot eliminate bacterial invasion Unique location of bacteria in hard tooth structure prevents them being eliminated by phagocytes Bacteria in dentinal tubules

26 Dendritic Cell: Ag Processing TLR6 TLR2 lysosome phagosome phagocytosis Antigen processing cells Dendritic cells Macrophages B lymphocytes Innate immune response

27 Dendritic Cell: Ag Processing endocytosis endosome MHC-II + CLIP MHC-II co-stimulatory molecule CD 86 lysosomal hydrolysis of peptides Peptide CLIP release binding by from MHC-II MHC-II

28 Adaptive Immunity Cell Mediated IFNγ, IL12 CD4+ T H T H 0 armed T H 1 Humoral Killer T antibodies naïve IL4,2,7 T H 2 B plasma lymph node

29 Caries: Immune Response caries Innate Response Finds pathogen Generic response to LTA & LPS Adaptive Response Pathogen specific attack neutrophil NK cell plasma cell killer cell T cells macrophage dendritic cell dendritic cell lymph node

30 Critical Juncture in Pulpitis Bacterial invasion of tertiary dentine Accumulation of neutrophils that discharge lysozymes to digest phagocytozed bacteria micro- abscess formation Lesion localized and walled off Trowbridge (1981)

31 Adaptive Tissue Response Cell-mediated immunity (cellular) Lactobacilli Actinomycosis Prevotella Humoral immunity (specific antibody) Reversible Pulpitis Irreversible Pulpitis

32 Adaptive Immune Response Can lead to irreversible pulpitis if caries is not removed Exaggerated inflammatory response microabscess formation Hahn & Liewehr (2007)

33 Vascular System Pulp has limited ability to withstand increase in pressure because of low compliant system Normal pulp does not function at 100% capacity Takahashi et al. (1982) Cat Premolar-Vascular Cast

34 Vascular System Numerous A-V shunts may open up in inflammation to reduce intrapulpal pressure Cat Premolar-Vascular Cast Kishin et al. (1989)

35 Vascular System Excess interstitial fluid from area of inflammation will be absorbed into the circulation and lymphatic system in the unaffected areas of the pulp

36 Vascular System If excess interstitial fluid from area of inflammation can not be absorbed into the circulation and lymphatic system increased intrapulpal pressure pain

37 Local Irritation Metabolic Wastes Accumulate, ph Local Inflammation Total Necrosis Local Necrosis Vascular Permeability Filtration Modified from Tjaderhane (2002) Blood Flow Oedema Venule Resistance LCS Swelling

38 Pulpal Response to Caries Response spreads apically as bacterial front advances

39 Apical Periodontitis Bacteria has no dentine tubules to provide a safe haven when they go beyond the apex Inflammatory response at the apex is effective Bacteria seldom encountered Nair (2000)

40 Apical Pathosis? Nair (2000) Abscess Granuloma Cyst

41 Chronic Hyperplastic Pulpitis Pulpal diagnosis: Asymptomatic irreversible pulpitis (Pulp polyp) Exuberant proliferation of chronically inflamed pulp Open carious lesions in children/young adults usually first permanent molars

42 Diagnostic Dilemmas

43 Sensitization in Pulpitis IL-1ß and TNF nociceptive threshold of afferents through PGs and NGF contributing to pain in pulpitis Normal LPS

44 Diagnostic Dilemmas Multirooted teeth could have different pulpal conditions in each root

45 Diagnostic Dilemmas Nerve fibers of the pulp are relatively resistant to necrosis (Mullaney 1970) C fibers are able to function when hypoxic (Torebjörk & Hanin 1973) Nerves can be sensitized

46 Histopathology & S/S Poor correlation between histopathological condition with clinical signs and symptoms Variation in human response/threshold to pain Variation in pathogens & their virulence

47 Bacteria & S/S High Lactobacilli Deep Caries Low Lactobacilli Hahn & Liewehr (2007) IL-10 & Treg Antiinflammatory Organic Acids High Prevotella Indole, Ammonia Super -antigens High Streptococci Pro-inflammatory cytokines Not sensitive to cold/heat Heat Sensitive Cold/Heat Sensitive

48 Root Canal Biofilm Environment Niche 1 Coronal Segment High O 2 tension Nutrients available from oral cavity Micro-organisms directly exposed to treatment action Chavez de Paz (2007)

49 Root Canal Biofilm Environment Niche 2 Main Canal Low O 2 tension Reduced amounts of nutrients from the oral cavity Micro-organisms directly exposed to treatment action Chavez de Paz (2007)

50 Root Canal Biofilm Environment Niche 3 Apical Segment Very low O 2 tension Nutrients available from periapical tissue Micro-organisms probably less affected by treatment measures Chavez de Paz (2007)

51 Bacteria in Root Canal Walls Challenge: How can we reliably destroy bacteria in their safe havens in the dentinal tubules? x5000 Sen et al. (1995)

52 Summary Pulpal and periapical pathosis is usually a continuum of (the infectious disease) caries The transition from one phase to another in the spread of pulpal and apical infection is not clear cut Clinical signs and symptoms may not accurately reflect the pulpal condition

53 Summary Variations in the manifestations of pulp and perapical disease will depend on the host response, and largely to the variation in the mix and virulence of the pathogens Understanding this will help in the diagnosis and prescription of the appropriate treatment for both pulpal and periapical diseases

54 The End