1. FACTORS AFFECTING RESPONSE OF PULP
1.1. Severity and duration of irritant.
1.2. Nature of irritant
1.3. Health condition of the pulp
1.4. Apical blood flow
1.5. Local anatomy of the pulp chamber
1.6. Host defence
2. CLASSIFICATION
2.1. According to pathological condition
2.1.1. Focal or acute reversible pulpitis (Pulp hyperaemia)
2.1.1.1. characterized by vascular dilatation
2.1.1.2. ETIOLOGY
2.1.1.2.1. Any mild pulp irritants like application of ice to tooth etc.
2.1.1.3. CF
2.1.1.3.1. sudden, mild-moderate pain.
2.1.1.3.2. Duration
2.1.1.3.3. Precipitating factors of pain
2.1.1.3.4. Nature of pain
2.1.1.4. HP
2.1.1.4.1. Dilated and congested blood vessels.
2.1.1.4.2. Presence of normal odontoblasts
2.1.1.5. PROGNOSIS
2.1.1.5.1. reversible conditio
2.1.1.5.2. If it is treated , pulp will return normal
2.1.1.5.3. If it is left untreated , it will enter the next phase (ACUTE PROGRESSIVE PULPITIS)
2.1.2. Irreversible pulpitis
2.2. According to its duration
2.2.1. Acute pulpitis
2.2.2. Acute progressive pulpits
2.2.2.1. CF
2.2.2.1.1. Duration
2.2.2.1.2. Precipitating factors of pain
2.2.2.1.3. Nature of pain
2.2.2.2. PROGNOSIS
2.2.2.2.1. If untreated, it will change to chronic pulpitis or pulp necrosis
2.2.2.3. HP
2.2.2.3.1. <—Congested venules
2.2.2.3.2. Necrotic zone – PMNLs & histiocytes.
2.2.3. Chronic pulpitis
2.2.3.1. CF
2.2.3.1.1. painful
2.2.3.1.2. Duration
2.2.3.1.3. Precipitating factors of pain
2.2.3.1.4. Nature of pain
2.2.3.2. HF
2.2.3.2.1. Varying sizes of dilated blood vessels.
2.2.3.2.2. Degenerated odontoblasts seen.
2.2.3.2.3. Chronic inflammatory cells and fibrosis.
2.2.3.3. PROGNOSIS
2.2.3.3.1. It is dependant on the success of pulp capping.
2.2.4. Chronic open hyperplastic (pulp polyr)
2.2.4.1. characterized by hyperplasia of connective tissue of pulp
2.2.4.1.1. in the form of polypoid mass
2.2.4.2. originates from exposed pulp chamber
2.2.4.3. CF
2.2.4.3.1. Site
2.2.4.3.2. Shape
2.2.4.3.3. Colour
2.2.4.3.4. Covering surface
2.2.4.4. HP
2.2.4.4.1. Granulation tissue
2.2.4.4.2. Generalized degenerated odontoblasts also called “Wheat Shafing” odontoblasts
2.2.4.4.3. Mass is covered by hyperplastic stratified squamous epithelial surface
2.3. According to presence of dentin covering the pulp chambe
2.3.1. Open pulpitis
2.3.2. Closed pulpitis
2.4. According to extension of inflammation
2.4.1. Partial pulpitis
2.4.2. Complete / total pulpitis
2.5. According to amount of pus formation
2.5.1. Exudative pulpitis
2.5.2. Suppurative pulpitis
3. INTRODUCTION
3.1. Pulpitis
3.1.1. inflmmation of pulp tissue - response to surrounding environment.
3.2. Tooth vitality
3.2.1. depends on defence response of pulp- dentin complex by
3.2.1.1. Sclerotic dentin
3.2.1.2. Tertiary dentin
3.2.1.3. Calcified bridge of dentinal tubules
4. ETIOLOGY
4.1. MECHANICAL
4.1.1. Trauma, iatrogenic damage and barometric changes.
4.2. THERMAL
4.2.1. uninsulated metallic restorations
4.2.2. dental procedures
4.2.2.1. cavity preparation, exothermic chemical reactions of dental materials
4.3. CHEMICAL
4.3.1. Irritation from certain dental materials or from erosion.
4.4. BACTERIAL
4.4.1. Through toxins or from direct extension of caries
5. PERIAPICAL tissue
5.1. PERIAPICAL GRANULOMA (Chronic apical periodontitis)
5.1.1. Chronically inflamed granulation tissue at the apex of a non vital tooth.
5.1.2. not static and may transform into periapical cysts or undergo acute exacerbation
5.1.3. CF
5.1.3.1. Initially – constant, dull & throbbing pain.
5.1.3.2. Later stages
5.1.3.2.1. mostly asymptomatic.
5.1.3.3. if acute exacerbation occurs:::
5.1.3.3.1. Pain & sensitivity can develop
5.1.3.4. No mobility or sensitivity to percussion
5.1.3.5. Pulp vitality tests are negative.
5.1.4. RGF
5.1.4.1. Well / poorly defined radiolucency
5.1.4.1.1. small / large
5.1.4.2. Loss of apical lamina dura
5.1.4.3. Root resorption is common
5.1.4.4. Cannot distinguish periapical granulomas from ????
5.1.4.4.1. periapical cysts on a radiograph.
5.1.5. HF
5.1.5.1. tissue containing a dense lymphocytic infiltrate mixed with PMNL’s
5.1.5.2. Epithelial rests of Malassez may be seen
5.1.5.3. Cholesterol clefts may also be seen
5.1.5.3.1. along with associated multinucleated giant cells.
5.1.5.4. Areas of extravasation of RBC’s and hemosiderin pigmentation
5.2. RADICULAR CYST (PERIPAICAL CYST / APICAL PERIODONTAL CYST)
5.2.1. radicular cyst arises from epithelial rests of Malassez
5.2.1.1. located in the PDL as a result of inflammation.
5.2.2. radicular cyst remains behind in jaws after removal of infected tooth – then called:?????
5.2.2.1. RESIDUAL CYST.
5.2.3. CF
5.2.3.1. Age
5.2.3.1.1. peak in 3rd, 4th and 5th decades. Old
5.2.3.2. Sex
5.2.3.2.1. Slightly more in males.
5.2.3.3. Site
5.2.3.3.1. Maxillary anterior region
5.2.3.4. Commonest cystic lesion of jaws.***
5.2.3.5. Signs & symptoms
5.2.3.5.1. Primarily symptom less.
5.2.3.5.2. Large cyst
5.2.3.5.3. Discovered accidentally during routine dental X ray exam.
5.2.3.5.4. if cysts breaks through cortical plates, lesion becomes???
5.2.3.5.5. Diagnostic criteria
5.2.3.5.6. Rare in deciduous teeth.
5.2.4. RGF
5.2.4.1. round / ovoid ‘lucency
5.2.4.1.1. sclerotic borders
5.2.5. DIFFERENTIAL DIAGNOSIS
5.2.5.1. Periapical granuloma
5.2.5.2. Peripaical cemento – osseous dysplasia (early lesions)
5.2.6. PATHOGENESIS
5.2.6.1. 1. PHASE OF INITIATION:
5.2.6.1.1. Epithelial rests of Malassez included within the developing periapical granuloma
5.2.6.2. 2.PHASE OF CYST FORMATION:
5.2.6.2.1. occur in two possible ways
5.2.6.3. 3. PHASE OF ENLARGEMENT:
5.2.6.3.1. Increase protein content as epithelium desquamates into lumen—>
5.2.6.3.2. Fluid enters the lumen to equalize the osmotic pressure
5.2.7. HP
5.2.7.1. non keratinized epithelium
5.2.7.2. Epithelium usually shows arcading around the CT
5.2.7.3. Hyaline / Rushton bodies
5.2.7.3.1. found in epithelium and rarely in CT wall.
5.2.7.3.2. These are curved or linear structures with eosinophilic staining properties.
5.2.7.4. Cholesterol crystals in from of clefts are often seen in the CT wall
5.2.7.5. Different types of dystrophic calcification are also seen in CT wall.
5.2.7.6. Keratinization if found
5.2.7.6.1. due to metaplasia
5.2.7.6.2. must not be confused with a KOT
5.3. PERIAPICAL ABSCESS (ACUTE DENTOALVEOLAR ABSCESS)
5.3.1. Collection of acute inflammatory cells at the apex of a non vital tooth
5.3.2. Acute lesions may arise either as
5.3.2.1. initial pathosis
5.3.2.2. acute exacerbation of a chronic periapical pathology
5.3.2.2.1. Called Phoenix abscess).
5.3.3. CF
5.3.3.1. Initial stages
5.3.3.1.1. tenderness
5.3.3.2. Later
5.3.3.2.1. pain becomes intense,
5.3.3.2.2. extreme sensitivity to percussion.
5.3.3.3. Extrusion of tooth in its socket.
5.3.3.4. Systemic findings
5.3.3.4.1. fever, malaise, chills.
5.3.3.5. Abscess may spread along path of least resistance through medullary spaces resulting in????
5.3.3.5.1. Osteomyelitis
5.3.3.6. perforate cortical bone and spread to soft tissues resulting in????
5.3.3.6.1. Cellulitis
5.3.3.7. granulation tissue – Parulis.
5.3.4. RGF
5.3.4.1. initial stage
5.3.4.1.1. thickening of periodontal ligaments.
5.3.4.2. Later
5.3.4.2.1. ill defined radiolucency.
5.3.5. HP
5.3.5.1. contains abundant PMNL’s mixed with inflammatory exudate, cellular debris and histiocytes.
5.3.5.2. Phoenix abscesses may also contain soft tissue component comprising of granulation tissue mixed with areas of abscess
5.4. CELLULITIS
5.4.1. rapidly spreading inflammation of the soft tissues characterized by diffuse pus formation.
5.4.2. happens if an abscess is not able to establish drainage
5.4.3. Types
5.4.3.1. infection spreads through tissue spaces
5.4.3.1.1. canine space, infratemporal space, pharyngeal space, buccal space, submental and submandibular space
5.4.3.2. arising from dental infection
5.4.3.2.1. spreading through soft tissues of head and neck can take various forms.
5.4.3.3. 1-Ludwig’s angina
5.4.3.4. 2-Cavernous sinus thrombosis
5.5. OSTEOMYELITIS
5.5.1. acute / chronic inflammatory process in medullary spaces or cortical surfaces of bones.
5.5.2. Tyoes
5.5.2.1. Acute suppurative osteomyelitis
5.5.2.1.1. occurs when acute inflammation spreads through medullary spaces of bone.
5.5.2.1.2. CF
5.5.2.1.3. HF
5.5.2.2. Chronic suppurative osteomyelitis
5.5.2.2.1. arise either de novo from the onset or as a continuation of acute osteomyelitis
5.5.2.2.2. CF
5.5.2.2.3. HP
5.5.2.3. Diffuse sclerosing osteomyelitis
5.5.2.3.1. pain, inflammation, varying degrees of periosteal hyperplasia, sclerosis and radiolucency of affected bone.
5.5.2.3.2. Can be confused clinically and radiologically with
5.5.2.3.3. CF
5.5.2.3.4. RGF
5.5.2.3.5. HP
5.5.2.4. Condensing osteitis (Focal sclerosing osteomyelitis)
5.5.2.4.1. refers to a focal area of bone sclerosis associated with apices of pulpally involved (caries, deep restorations or pulp necrosis) teeth.
5.5.2.4.2. To be diagnosed as condensing osteitis, association with inflammation is essential
5.5.2.4.3. CF
5.5.2.4.4. HP
5.5.2.4.5. DIFFERENTIAL DIAGNOSIS
5.5.2.5. Osteomyelitis with proliferative periostitis
5.5.2.5.1. called Periostitis ossificans or Garrѐ’s Osteomyelitis.
5.5.2.5.2. type of osteomyelitis associated with periosteal bone formation.
5.5.2.5.3. CF
5.5.2.5.4. HP
5.5.2.6. Alveolar osteitis (Dry socket / Fibrinolytic alveolitis)
5.5.2.6.1. blood clot at the extraction site fails to organize which eventually leads to delayed healing and causes a condition called “Dry socket”.
5.5.2.6.2. due to transformation of plasminogen to plasmin with resultant lysis of fibrin and formation of kinin (pain mediators).
5.5.2.6.3. PREDISPOSING FACTORS:
5.5.2.6.4. CF
5.5.3. PREDISPOSING FACTORS
5.5.3.1. After odontogenic infections
5.5.3.1.1. Trauma to jaws