causes of pulp and periapical disease (part 1)_62353991f6779a54d5746320c9164ed3.pptx

Causes of pulp and periapical injuries BDS 11129 Date : xx / xx / xxxx Aims: The educational aims of this lecture are: To explain types of endodontic infections To detail the etiology and progress of pulp and periapical injuries To explain the pulp and surrounding tissues response to pulp and per...

Causes of pulp and periapical injuries BDS 11129 Date : xx / xx / xxxx Aims: The educational aims of this lecture are: To explain types of endodontic infections To detail the etiology and progress of pulp and periapical injuries To explain the pulp and surrounding tissues response to pulp and periapical injuries Objectives: On completion of this lecture, the student should have: An understanding of different injuries of the pulp An understanding of how pulp and periapical injuries develop An understanding of what causes pulp and periapical injuries Living irritants (microbial) Main irritants of the pulp Physical irritation Electrical irritation Thermal irritation Non living irritants Chemical irritation Bacteria was found to be the main cause of pulp and periradicular infection. Pathways of pulp and periradicular infection: 1. Exposed dentinal tubules: due to caries, leaky restoration, fracture, crack, periodontal pocket, attrition, abrasion or naturally-absent cementum and enamel at cemento-enamel junction. 2. Direct pulp exposure due to caries, restorative procedure, fracture. 3. Lateral canals due to periodontal disease with deep pockets. 4. Apical foramen due to periodontal disease with deep pockets. 1- Living irritants (Microbial): • Bacteria and their by-products • Caries is the most common cause of ingress of bacteria to pulp • Response depends on No. of MO x Virulence / Tissue resistance Lets take a closer look on microbial ecology Types of endodontic infection: 1. Intraradicular: infection inside root canal. It can be divided into: a. Primary b. Secondary c. Persistent infection 2. Extraradicular: infection outside of root canal. 1.Intraradicular Endodontic Infection: a) Primary infection: The first microorganisms which invade and colonize necrotic pulp. It is mixed polymicrobial infection, mainly containing: • Anaerobic bacteria. • Facultative micro-organisms. • Obligate anaerobes especially G-ve bacteria. b) Secondary infection:  Micro-organisms are introduced in root canals during treatment, between appointments and after root canal obturation.  It consists of mixed infection as 1ry infection. Clinical problems: 1- Persistent exudation and symptoms. 2- Interappointment Flare ups. 3- Failure of endodontic c) Persistent infection:  It consists of resistant irrigation and medication. micro-organisms to  They can endure nutrition deprivation, so they cause persistent or recurrent infection leading to endodontic failure.  It consists of micro-organisms as primary or secondary infection but fewer species, with increase in G+ve facultative anaerobic especially Enterococcus Faecalis and fungi (Candida Albicans). 2. Extraradicular infection: In periradicular area may be caused by: Intrardicular infection that extends to periapical area e.g. Acute apical abscess caused by necrotic pulp It contains micro-organisms similar as their intraradicular source, but with increase in Gram -ve anerobic bactereia of bacteroids as: Prevotella (denticolla, intermedia, nigrescens) and Porphyromonas (endodontalis, gingivalis) Patterns of microbial colonization: free floating single micro-organisms in an aqueous environment inside root canal which can cause infection. 1- Planktonic form Same species  aggregates Different species  Coaggregates 2Grouping It is formed by bacterial adherence to dentin, colonization & multiplication. 3Biofilms • Sessile biofilms are aggregates of one or more species of bacteria in a matrix that they synthesize and that attaches the micro-organism to a solid surface (e.g tooth surface). Mechanism of microbial pathogenicity and virulence factors Stages in development of an endo-infection A successful pathogen, can: RE COLONIZE SURVIVE PROPAGATE EVADE induce DAM Mechanism of microbial pathogenicity and virulence 1- factors Bacterial biofilms: i) Resistant to antimicrobial agents ii) Can’t be removed by mechanical preparation alone iii) Inside biofilms bacteria may be synergistic or antagonistic 2- Cellular components of microorganisms: Fimbrie (pilli) Capsule Extracellular vesicles Allow adherence of bacteria to surfaces & allow aggregation In gram +ve/-ve Protects bacteria from phagocytosis In cytoplasm of gram –ve Bind to antibodies or contain enzymes Mechanism of microbial pathogenicity and virulence factors 3- Microorganisms’ secreted by products: a) Enzymes Neutralize Igs Aid in the spread of MO Eg. Protinases, Collagenase Hyaluronidase, Fibrinolysin Mechanism of microbial pathogenicity and virulence factors 3- Microorganisms’ secreted by products: b) Endotoxins  Lipopolysaccharides  component of outer membrane of gram –ve bacteria only  Released after death of the MO  Activates complement system  fever, shock & bone resorption  Increases in symptomatic cases c) Exotoxins  Polypeptides  produced in the cytoplasm of gram +ve bacteria mainly  Secreted by living Mos  Leukotoxin  creates small holes in leukocyte membrane  cell lysis 2- Non Living irritants (Iatrogenic): I- Physical: 1- Pressure → Pressure→ Friction→ Heat which will lead to pulpal irritation 2- Speed (RPM) → most dangerous 3000-30000 RPM ( needs the application of more pressure) 3- Depth of cutting → Remaining dentin thickness (2mm thickness is safest as dentine is best insulator) 4- Presence or absence of an insulating base 5- Other physical factors: a) Loss of enamel b) High filling ( cause frequent pulpal trauma) c) Hot impression d) Orthodontic TTT II- Thermal 1- Pressure 2- Speed 3- Type of cutting inst → abrading are the most dangerous (due to broader surface area) 4- Coolants → Air-water spray → dentin thickness 0.3mm III- Chemicals 1- For cleaning the cavity eg. Phenol ( pulp irritation), ether & chloroform (desiccation), hydrogen peroxide . 2- Used during filling eg. acid etch/ polymerization shrinkage of composites 3- Traumatic: May be accompanied by fracture of crown &/or root. Accidental May be Iatrogenic Response may be one of the following: Healing Calcification Necrosis 4- Idiopathic: ( internal resorption) PULP AND PERIAPICAL DISEASES I-Classification of pulp inflammation 1- According to severity & duration: Chronic (Granulation tissue) Acute (Exudate) 2- According to presence or absence of symptoms: Symptomatic Asymptomatic 3- According to the ability to heal: Reversible Irreversible Reversible pulpitis level of pulp inflammation in which tissue is capable to return to normal state if the irritant is removed Irreversible pulpitis a higher level of inflammation in which dental pulp has been damaged beyond the point of recovery PULPAL IRRITATION PULPAL INFLAMMATION NOT TREATED PULPAL NECROSIS NOT TREATED PERIAPICAL PATHOSIS Pulpal Diseases I- Inflammatory: 1- Hyperaemia 2- Acute Pulpitis 3- Chronic Pulpitis II- Additional : 1- Necrosis 2- Retrogressive pulp changes I- Atrophy II- Calcification 3- Internal resorption In all diseases • Definition • Pathogenesis I- Visual II- Signs & Symptoms • Examination & diagnosis→ III- Percussion IV- RG V- Sensitivity • Treatment Pulpal Diseases I- Inflammatory: 1- Hyperaemia ( reversible pulpitis) 2- Acute Pulpitis 3- Chronic Pulpitis Pulpal Diseases I- Inflammatory: 1- Hyperaemia (Reversible pulpitis) 1- Definition: • Reversible pulpitis is a clinical condition associated with subjective and objective findings indicating presence of mild inflammation in the pulp tissue. If the cause is eliminated, inflammation will reverse and the pulp will return to its normal state Local vasodilatation→ ↑ Vascular permeability→ Oedema 2- Pathogenesis: VD→↑ Vascular permeability→ Fluid exudate (odema) 3- Examination & diagnosis: I- Visual: incipient Caries, Deep filled cavity or Recent trauma, cervical erosion, or occlusal attrition ( mild stimuli) II- S&S: Pain: sharp, brief duration (not spontaneous) III- Percussion: -ve IV- RG: normal V- Sensitivity: 1- Thermal: +ve 2- Electric: +ve at low current 4- Treatment: TTT of the cause (The removal of irritants and sealing and insulating the exposed dentin) Pulpal Diseases I- Inflammatory: 2- Acute pulpitis (Irreversible pulpitis) (Hot tooth) 1- Definition: • A clinically detectable, painful & irreversible acute inflammatory response of the pulpal CT to an irritant in which exudates are hyperactive & play a dominant role. It is often a sequel to and a progression from reversible pulpitis 2- Pathogenesis: 1- VD→↑ Vascular permeability→ Fluid exudate 2- Slow blood flow and increased blood viscosity 3- ↑IP pressure & pain 5- Spread of inflammation Stages: 1- Early: Hot & Cold→ pain (C & A delta fibers) 2- Advanced: Hot→ pain (C-fibers) Cold→ relieves pain Pulpal Diseases I- Inflammatory: 2- Acute pulpitis (Irreversible pulpitis) (Hot tooth) 3- Examination & diagnosis: I- Visual: Caries, Deep filled cavity or Recent trauma II- S&S: Pain: sharp throbbing (spontaneous) Lingers ↑ at night Diffused or referred III- Percussion: -ve IV- RG: normal V- Sensitivity: 1- Thermal: depends on the stage 2- Electric: +ve at low current 4- Treatment: RCT 1- Early: Hot & Cold→ pain 2- Advanced: Hot→ pain Cold→ relieves pain Differential diagnosis between hyperemia and acute pulpitis: Reversible Pulpitis Irreversible Pulpitis 1- Caries Present Present & deep 2- Pain Momentary & not spontaneous Lingers & spontaneous Pulpal Diseases I- Inflammatory: 3- Chronic pulpitis 1- Definition: • Inflammatory response of pulpal CT to an irritant in which proliferative forces are hyperactive & play a dominant role. (proliferation = granulation tissue) • It is a chronic inflammatory reaction of the pulp that may result from long-term, low grade injury [When the irritant is not severe enough to cause acute infection] 2- Pathogenesis:  When organisms are of low virulence. Slowly progressing caries. May develop as a sequel of acute pulpitis • It is asymptomatic as there is an Outlet for exudate ( carious cavity, venous or lymphatic circulation) • NB. Outlet closed→ Pain Chronic Pulpitis 1-Chronic Closed Pulpitis 2-Chronic Open Pulpitis A-Chronic Open Ulcerative Pulpitis B-Chronic Open Hyperplastic Pulpitis 1-Chronic closed pulpitis: Clinical Features: I- Visual: Caries, Deep filled cavity II- S&S: Pain: The tooth may exhibit intermittent dull aching pain. ( pain is poorly localized) III- Percussion: -ve IV- RG: normal V- Sensitivity:  1- Thermal: Sensitivity to heat and cold is less than that in acute pulpitis [due to degeneration of nerve fibers] 2- Electric: +ve at higher current 4- Treatment: RCT 2-Chronic open pulpitis: Is a condition in which the pulp chamber is open to the oral cavity [large portions of the crown are usually missing] A-Chronic open ulcerative pulpitis: Clinical features  Symptoms range from non to a minimum, with slight pain of a dull character made worse by thermal changes.  Edema in the pulp [which causes pressure and chemical irritation to the nerve endings] escapes from the superficial part of the tissue through the exposure.  So symptoms may be decreased or disappeared B-Chronic Open Hyperplastic pulpitis (pulp polyp) It is a special form of chronic pulpitis that occurs in: • The molar teeth (primary and permanent) of children and young adults. • The involved teeth exhibit large carious lesions that open into the coronal pulp chamber. Clinical Features  Pulp polyp appears as a red or pinkish soft nodule protruding into the cavity.  It is painless (as there is no exudate under pressure) but may be tender and bleed on probing. Pulpal Diseases I- Inflammatory: 1- Hyperaemia 2- Acute Pulpitis 3- Chronic Pulpitis 4- Subacute II- Additional : 1- Necrosis 2- Retrogressive pulp changes I- Atrophy II- Calcification 3- Internal resorption 4- Previously treated tooth Pulpal Diseases II- Additional: 1- Necrosis: 1- Definition: Death of the pulp (inflammation or circulation arrest) It is a sequel of : A) Acute and chronic inflammation. B) Immediate arrest of circulation due to traumatic injury. C) It could be either complete or partial. 2- Pathogenesis: Classification: 1- Liquefactive: - Good blood supply (i.e. acute or chronic inflammation) - Pus formation 2- Coagulative: - Poor blood supply (Trauma) - Soft solid cheesy like mass (caseation) Pulpal Diseases II- Additional: 1- Necrosis: 3- Examination & diagnosis: I- Visual: Hx of caries or trauma, dark colored II- S&S: Painless III- Percussion: -ve IV- RG: normal or slight widening of PMS V- Sensitivity: 1- Partial necrosis: False +ve 2- Electric: False +ve (Liquefactive) 4- Treatment: RCT (multiple visits) Pulpal Diseases II- Additional: 2- Retrogressive pulp changes: I- Atrophy 1- Definition: wasting away or decrease in size 2- Pathogenesis: 1- ↓ No. of cells 2- ↓ Ground substance 3- ↑ Mature collagen fibers Pulpal Diseases II- Additional: 2- Retrogressive pulp changes: I- Atrophy: 3- Examination & diagnosis: I- Visual: Hx of caries, attrition, erosion or trauma II- S&S: Painless III- Percussion: -ve IV- RG: normal or slight widening of PMS V- Sensitivity: -ve or slight response at high current 4- Treatment: may be left untreated unless the patient complains Pulpal Diseases II- Additional: 2- Retrogressive pulp changes: II- Calcification (Chalky tooth) 1- Definition: Ca deposits in the pulp chamber 2- Pathogenesis: Classification 1- Pulp stone (denticles): in pulp chamber may classified according to: a) Location: Attached Free b) Structure: True denticles ( composed of dentine) 2- Diffuse calcification: in RC Embedded False denticles ( deposition of calcium salts in dead or degenerated tissue) Pulpal Diseases II- Additional: 2- Retrogressive pulp changes: II- Calcification (Chalky tooth) 3- Examination & diagnosis: I- Visual: Hx of caries, attrition, erosion or trauma, chalky appearnce II- S&S: Painless III- Percussion: -ve IV- RG: calcific changes could be seen(A reduction in coronal pulp space followed by a gradual narrowing of the root canal V- Sensitivity: -ve or slight response at high current 4- Treatment: may be left untreated 3- Internal Resorption: Inflammation in the pulp may initiate resorption of adjacent hard tissues. 4- Previously Treated Pulp: • This condition represents a clinical diagnostic category in which the tooth has had either partial or complete endodontic therapy. • The teeth in this category can be symptomatic or asymptomatic, depending on pulpal and periapical conditions. • Completion of partial root canal therapy or retreatment of failed root canal treatment, endodontic surgery, or extraction is indicated for these teeth. Aims: The educational aims of this lecture are: To explain types of endodontic infections To detail the etiology and progress of pulp and periapical injuries To explain the pulp and surrounding tissues response to pulp and periapical injuries Objectives: On completion of this lecture, the student should have: An understanding of different injuries of the pulp An understanding of how pulp and periapical injuries develop An understanding of what causes pulp and periapical injuries Reading material: Students are advised to read details at: 1. Cohen`s pathways of the pulp, 11th edition, 2016, Kenneth M. Hargreaves and Louis H. Berman. (chapters 14 and 15) 2. Endodontic science (two volumes), 2nd edition, 2009, Carlos Estrela. (chapters 8 and 9) 3. Problems in endodontics, Etiology, diagnosis and treatment, 2009, Michael Hulsmann and Edgar Thank you