1. General Info
1.1. 1. Pulp Definition
1.1.1. 1. Delicate C.T with blood vessels, lymphatics,nerves, UMCs and Histiocytes
1.1.2. 2. Histiocytes: special cells with cytoplasmic extension and oval nuclei with coarse granular chromatin; in inflammation they withdraw their processes and become macrophages
1.1.3. 3. number of histiocytes decrease in old age thus they have less resistance to infection
1.2. 2. Significan of Pulp Anatomy in inflammation
1.2.1. 1. Enclosed
1.2.1.1. 1. pulp is enclosed with walls of dentine, preventing swelling when inflamed
1.2.2. 2. Small Apical Foramen
1.2.2.1. 1. nerves and blood vessels pass through small apical foramen.
1.2.2.2. 2. irritant cause arteries to dilate, making veins constrict ;draining inturn decreases.
1.2.2.3. 3. As long as veins are capable to drain no harm occurs
1.2.2.4. 4. if pressure is too great that veins are completely constricted causing congestion, degeneration, necrosis
1.2.3. 3. No Collateral Circulation
1.2.3.1. 1. Blood can't reach pulp from another source
1.2.3.2. 2. it weakens the defensive mechanism
1.2.4. 4. Temperature Effect
1.2.4.1. 1. pulp responds to temp changes below 20 and above 45 degree producing hyperemia (increased blood) and inflammatory changes
1.2.5. 5. No Power of Generation
2. Ateiology
2.1. 1. Normally
2.1.1. 1. pulp surrounded by dentine and enamel
2.1.2. 2. as long as they are intact, they provide protection to pulp
2.1.3. 3. they act as a physical barrier to harmful solutions and insulators to temperature changes
2.2. 2. Irritant Classification
2.2.1. 1. Grp 1
2.2.1.1. 1. Living irritants (microbial)
2.2.2. 2. Grp 2
2.2.2.1. 1. Non Living irritants
2.2.2.1.1. 1. Physical
2.2.2.1.2. 2. Chemical
2.3. 3. N.B
2.3.1. 1. some operative procedures endager health of pulp more than disease
2.3.2. 2. decay is less harmful than operative procedures used to treat it
2.3.3. 3. pulp inflammation caused by dentist's is called Odonto-Iatro-genic Pulpitis
3. Living Irritants (Microoraganisms )
3.1. 1. Main source of pulp irritation
3.2. 2. Gain Entrance through
3.2.1. 1. Open Cavity
3.2.1.1. 1. Fracture
3.2.1.1.1. 1. due to trauma or fracture of crown causing pulp exposure which allows bacteria to enter
3.2.1.2. 2. Operative Procedure
3.2.1.2.1. 1. Due to Operative procedures that accidentally exposes pulp; unless controlled by pulp capping
3.2.1.3. 3. Caries
3.2.1.3.1. 1. caries allows bacteria to invade by causing exposure
3.2.1.4. 4. Dentinal Tubules
3.2.1.4.1. 1. Invation through dentinal tubules may occur before cavitation by strept. , staph, lactobacilli and filamentous MO
3.2.2. 2. Gingival Cervice (Via PDL membrane)
3.2.2.1. 1. in Pdl disease MOs are present in pocket areas close to periapical regions and they may reach and infect pulp
3.2.3. 3. Extension from adjacent infected tooth
3.2.3.1. 1. as bacteria affecting one tooth find a way to adjacent sound tooth through blood or lymph
3.2.4. 4. Haematogenous Infection
3.2.4.1. 1. Bacteria in blood stream during bacteremia find way to pulp and localize and cause infection
3.2.4.2. 2. present in diseases as tonisilitis, prostatis, periodontitis (10%) and TB
3.2.4.3. 3. Ana-choresis is Phenomenon when bacteria circulating in blood tend to localize in inflamed areas
3.2.4.4. 4. Infected Pulp called Anachorectic pulpitis or Idiopathic pulpitis
4. Non Living Irritants
4.1. 1. Mechanical
4.1.1. 1. Accidental
4.1.1.1. 1. fracture of tooth crown or root
4.1.2. 2. Odonto-Iatro-genic
4.1.2.1. 1. Accidental Pulp Exposure
4.1.2.2. 2. Grinding of tooth surface
4.1.2.3. 3. Rapid Seperation of teeth
4.1.2.4. 4. Modern high speed instrument
4.1.2.5. 5. Traumatic Faulty occlusion
4.1.2.5.1. 1. restoration not in correct occlusal relationship with opposing
4.1.2.5.2. 2. causes breakdown of pdl and may involve pulp
4.2. 2. Thermal Irritation
4.2.1. 1. sudden temp change range from 20 degree to 45 degree
4.2.2. 2. Odonto-Iatrogenic
4.2.2.1. 1. Excess Heat generation by bur or stone during grinding and cavity preparation
4.2.2.2. 2. rapid polishing of teeth or restoration
4.2.2.3. 3. large metal filling with insufficient lining
4.2.2.4. 4. prolonged contact of thermal pulp tester
4.3. 3. Electrical
4.3.1. 1. Galvanic shock
4.3.1.1. 1. due to different electromotive potential (Gold and Amalgam)
4.3.1.2. 2. when they occasionaly come in contact intermit electrical current is set up
4.3.1.3. 3. if irritation is prolonged necrosis may occur
4.3.1.4. 4. thus one filling must be removed
4.4. 4. AER-ODON-Talgia
4.4.1. 1. tooth ache occuring to flying crew members at high altitudes or in low pressure chambers
4.4.2. 2. occur in vital pulp with caries or filling
4.4.3. 3. in treating them care should be taken to avoid pulp irritation from heat during drilling
4.4.4. 4. recommended to insert Zn-oxide in cavity after preparation to prevent pain
4.5. 5. Chemical
4.5.1. 1. due to Drugs, acid , saliva, food ingredients
4.5.2. 2. excess gingival recession exposes cementum to chemical agents found in some food
4.5.3. 3. acidic products in carious cavities
5. Disease of Pulp Classification
5.1. According to Type of inflammation
5.1.1. focal reversible pulpitis
5.1.2. acute pulpitis
5.1.3. chronic pulpitis
5.2. According to Extent of involvement
5.2.1. partial pulpitis/subtotal
5.2.1.1. inflammatory process confined to portion of pulp (pulp horn or coronal portion)
5.2.2. total pulpitis/ Generalized
5.2.2.1. entire pulp involved
5.3. According to Direct communication between pulp and oral enviroment
5.3.1. Open pulpitis
5.3.1.1. pulp communicate with oral cavity
5.3.2. closed pulpitis
5.3.2.1. no direct communication between pulp and oral cavity
6. Focal Reversible Pulpitis
6.1. 1. Definition
6.1.1. 1. earliest form of pulpitis
6.1.2. 2. referred to as pulp hypermia
6.1.3. 3. it is a reversible condition if irritant removed
6.2. 2. Clinical Features
6.2.1. 1. tooth is sensitive to thermal change specially COLD
6.2.2. 2. pain disappears after irritant is removed
6.2.3. 3. Tooth usually has
6.2.3.1. 1. deep carious lesion
6.2.3.2. 2. OR large metallic restoration with insufficient isolation
6.2.3.3. 3. OR restoration with defective margins
6.3. 3. Histological features
6.3.1. 1. dilatation of pulp vessel
6.3.2. 2. inflammatory fluid exudate
6.3.2.1. 1. due to increased passage of fluid through dilated vessels
6.3.3. 3. Haemoconcentration and increased viscosity of blood due to escape of Fluid Exudate
6.3.4. 4. Thrombosis in blood vessel may occur due to:
6.3.4.1. 1. Accumulation of IFE increases pressure outise
6.3.4.2. 2. slow blood flow and haemoconcentration
6.3.4.3. 3. may cause death of pulp
7. Acute Pulpitis
7.1. 1. definition
7.1.1. 1. acute inflammation of pulp rapidly after hyperemia
7.1.2. 2. if invading organism is viruelent and reistance is lowered
7.1.3. 3. may occur as an acute exacerbation of chronic inf. process
7.2. 2. Clinical Features
7.2.1. 1. all cardinal signs of Inflammation except swelling ( Red, Hot, Pain)
7.3. 3. Microscopic Featues
7.3.1. 1. it is a dynamic process
7.3.2. 2. irritant must reach certain strength before causing inflammation
7.3.3. 3. it's appearance is that of non specific inflammation.
7.3.4. 4. 1st reaction occurs when caries reach DEJ.
7.3.5. 5. mainly limited to part of pulp below carious dentinal tubules (partial acute pulpitis )
7.3.6. 6. 1st change is vascular dilatation
7.3.6.1. 1. capillaries become apparent due to increases blood flow
7.3.7. 7. 2nd stage: Swelling of Odontoblastic nuclei
7.3.7.1. 1. due to osmotic imbalance
7.3.8. 8. Afterwards
7.3.8.1. 1. disintegration of nuclei
7.3.8.2. 2. congestion of blood vessels
7.3.8.3. 3. pavementing of PMNLs on walls of widened vessles
7.3.8.4. 4. migration of cells to surrounding tissue
7.3.8.5. 5. fluid leaks out of cappilaries and seens as vesicles between cells
7.3.8.6. 6. oedema only compress tissue as pulp can't expand
7.3.8.7. 7. leucocytes confined to localized area rest of pulp is normal
7.3.8.8. 8. increased irritation may cause abscess
8. Pulp Abscess
8.1. 1. Clinical Features
8.1.1. 1. Pain either severe continous throbbing or less severe intermittent attacks
8.1.2. 2. severity increases when patient is lying down and with change of temperature
8.1.3. 3. In pulp inflammation edema is confined to chamber of dentine thus pressure is greater than in soft tissue
8.1.4. 4. products of inflammation as Histamine stimulate nerve endings producing pain
8.1.5. 5. Electric Vitality test produces a reaction at far low threshold than normal
8.1.6. 6. treated by removal of cause and Root Canal
8.2. 2. Microscopic Features
8.2.1. 1. usually occur when entrance to pulp is narrow and not enough drainage present
8.2.2. 2. number of PMNLs increases
8.2.3. 3. leukocytes are found beneath area of penetration or deeper within pulp tissue
8.2.4. 4. many leucocytes become necrotic and die releasing proteolytic enzymes
8.2.5. 5. Proteolytic enzymes dissolve pulp tissue causing LIQUEFACTION NECROSIS and PUS
8.2.6. 6. surrounding the abscess there is an area of dense mass of lymphocytes, plasma cells, monocytes
8.2.7. 7. bacteria is only present within abscess and the nearest layer (associated with necrotic cells
8.2.8. 8. Near these cells there is collagen wall (fibrous wall) that act as a barrier to infectious material
8.2.9. 9. toward normal pulp there is dilated vessels
8.2.10. 10. Abscess can be in several parts and eventually whole pulp is transferred to mass of dead tissue this is termed
8.2.11. 11. TOTAL SUPPURATIVE PULPITIS : suppurative exudate (pus and bacteria) are not localized and whole pulp involved
9. Chronic Pulpitis
9.1. 1. Definiton
9.1.1. 1. follow injury similar to those causing acute pulpitis (similar etiology)
9.1.2. 2. however irritant has low virulence so response is mild
9.2. 2. Etiology
9.2.1. 1. sequel to acute Pulpitis
9.2.2. 2. when irritant is not severe enough to cause acute infection
9.2.2.1. 1. low virulence organism
9.2.2.2. 2. caries progress slowly
9.2.3. 3. pulp is capped after traumatic exposure
9.2.4. 4. caries not completely removed from cavity
9.2.5. 5. may be in normal teeth affected by caries due to heamtogenous infection
9.3. 3. Classification
9.3.1. 1. Chronic Closed Pulpitis
9.3.2. 2. Chronic Open pulpitis
9.3.2.1. 1. ulcerative type
9.3.2.2. 2. hyperplastic type (pulp Polyp)
9.4. 4. Clinical Features
9.4.1. 1. tooth has intermittent dull aching pain
9.4.2. 2. lower sensitivity to hot and cold than in acute stage
9.4.3. 3. tooth needs higher responds to higher volt of electric pulp tester than normal (less sensitive)
9.5. 5. Mechanism and microscopic features
9.5.1. 1. reparative process in addition to destructive changes occur
9.5.2. 2. Bactrerial toxin in caries reach pulp through lymph in dentinal tubules
9.5.3. 3. toxins not strong enough to destroy odontoblast, only irritates it
9.5.4. 4. odontoblast lay down 2ry (reparative dentine)
9.5.5. 5. tubules are sealed by hyaline or calcified layer
9.5.6. 6. more or less irregular 2ry dentine laid down which reduces access of irritants and inflammation may resolve completely
9.5.7. 7. small number of bacteria enter pulp( Pioneers)
9.5.8. 8. if defense is strong and caries process is slow, degree of inflammation may be too mild to be recognized
9.5.9. 9. when qualitative and quantitative change occurs picture is seen as
9.5.9.1. 1. leucocytes in large numbers specially lymphocytes and plasma cells
9.5.9.2. 2. small abscess formation
9.5.10. 10. capillaries prominent
9.5.11. 11. fibroblastic activity evident
9.5.12. 12. collagen fibres seen in bundles ( as an attempt to wall off infected area)
9.6. 6. treatment
9.6.1. 1. root canal or extraction
10. Chronic Open Hyperplastic Pulpitis (Pulp Polyp)
10.1. 1. definition
10.1.1. 1. form of chronic pulpitis occur as either chronic exacerbation or new chronic onset
10.1.2. 2. paritcularly present in decideous molars with extensive carious lesion causing wide exposure of pulp)
10.2. 2. Clinical Features
10.2.1. 1. globular mass of tissue is protruding from pulp chamber
10.2.2. 2. pinkish or dark fleshy red color
10.2.3. 3. usually in children or young adult with large apical foramen and high blood supply, mostly deciduous molars and 6
10.2.4. 4. in early polyp it bleeds easily and there is slight but continuos offensive discharge (Bad Odor)
10.2.5. 5. later it may be penduculated, lobulated and look similar to gingiva micro and macroscopically
10.2.6. 6. this is because of implantation of new epithelial cells on its surface and then grow on it
10.2.7. 7. the covering help protect nodule of pulp from infection
10.2.8. 8. inflammation decrease and granulation tissue becomes collagenous fibrous tissue
10.2.9. 9. usually painless on sensation as hyperplastic rissue has few nerves
10.2.10. 10. lesion may or may not bleed easily depending on vascularity
10.3. 3. Microscopically
10.3.1. 1. granulation tissue covered by epithelium due to implantation of epithelial cells on surface
10.3.1.1. 1. source
10.3.1.1.1. 1. desquamated epithelial cells carried by saliva
10.3.1.1.2. 2. rubbing against buccal mucosa tongue or ginigva
10.3.2. 2. epithelium is stratified squamous and resemble oral mucosa with well formed rete pegz and keratinzed surface
11. Chronic Ulcerative Pulpitis
11.1. G. Info
11.1.1. 1. entire pulp or great part show chronic inflammatory changes
11.2. 2. Clinical
11.2.1. 1. symptomes are none to minimum pain (dull) worsened by thermal change
11.3. 3. Microscopic
11.3.1. 1. oedema escpes from superficial part through exposure
11.3.2. 2. in area of carious pulp exposure tissue is replaced by granulation tissue infiltrated with lymohocytes macrophaed and chronic inf.cells
12. Pulp Necrosis and Pulp Gangrene
12.1. G. Info
12.1.1. 1. untreated pulpitis lead to death of pulp
12.1.2. 2. inflammatory exudate compressed in enclosed dentine causes constriction of blood vessels (apical) causing infection and necrosis
12.2. 3. clinically
12.2.1. 1. necrosis causes cessation of all symptoms (no nerve supply to dead tissue)
12.3. 4. Microscopically
12.3.1. 1. empty pulp chamber and canals or isolated areas of necrotic structureless mass