Periapical  pathology 22 (1)
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Periapical  pathology 22 (1) Periapical pathology 22 (1) Presentation Transcript

  • PULP AND PERIAPICAL DISEASES  Submitted by Hina bhatia (521)
  • Contents  Introduction  Pathobiology of periapex  Acute and chronic  Inflammation Vs Immunology  Classifications of pulpoperipaical pathoses  Clinical signs and symptoms
  •  Healing mechanisms  Differential diagnosis  Ludwig’s angina , Cellulitis  Osteomyelitis , Periapical actinomycosis  Foreign body reactions  Conclusion Contents
  • Introduction
  • Apical Pulp tissue  less cellular  more fibrous  whitish in colour  large conc of glycogen →anaerobic environment  higher conc of sulfated glycosaminoglycans  fibrous tissue ~ PDL
  • Apical dentin  Less tubular , more amorphous , irregular  Sclerotic dentin increases with age  Odontoblasts of the pulp are absent/flattened/cuboidal  Optically transparent  Less permeable
  • Pathways of infection Opening in dental hard tissue wall caries clinical procedures trauma induced fractures microcracks Bacteria from the gingival sulcus/ P.pocket Endodontic reinfection Anachoresis
  • HOST ALLERGEN
  • HOST ALLERGEN Inflammation Phagocyte system Lymphatic system / T & B cells Immune/complement system Neural mechanism chemotaxis Endotoxins Exotoxins Enzymes PUS / tissue damage Stimulation of clast cells
  • Exudate (inflam edema)- pain Acute (exudative) Chronic (proliferative)
  • Classification by Franklin.s.weine Perapical pathosis of pulpal origin: 1.Painful pulpoperiapical pathoses a. Incipient acute apical periodontitis b. Advanced ’’ ’’ ’’ (i) acute periapical abscess (ii) recrudescent / phoenix abscess (iii) subacute peiapical abscess 2. Non painful periapical pathoses a. Pulpopariapical osteosclerosis(condensing osteitis) b. Incipient chronic apical periodontitis c. Advanced ’’ ’’ ’’ (i) periapical granuloma (ii) chronic periapical abscess (iii) periapical cyst
  • Hirsch et al (1979) – surgically excised pulpoperiaical lesions I. Periapical granuloma II. Epithelial granuloma III. Radicular cyst with modern (chronic inflammation) IV. Radicular cyst with strong ( acute or subacute ) inflammation and epithelial necrosis V. Radicular cyst without inflammation (chronic or acute)
  • WHO(1995) CLASSIFICATION Code number CATEGORY K04.4 K04.5 K04.6 K04.60 K04.61 K04.62 K04.63 K04.7 K04.8 K04.80 K04.81 K04.82 Acute apical periodontitis Chronic ’’ ’’ (periapicalgranuloma) Periapical abscess with sinus Periapical abscess wth sinus to maxillary antrum ’’ ’’ ’’ to nasal cavity ’’ ’’ ’’ to oral cavity ’’ ’’ ’’ to skin Periapical abscess without sinus Radicular cyst(apical periodontal cyst, periapical cyst) Apical and lateral cyst Residual cyst Inflammatory paradental cyst
  • Classification by Franklin.s.weine Perapical pathosis of pulpal origin: 1.Painful pulpoperiapical pathoses a. Incipient acute apical periodontitis b. Advanced ’’ ’’ ’’ (i) acute periapical abscess (ii) recrudescent / phoenix abscess (iii) subacute peiapical abscess
  • Painful pulpoperiapical pathoses Early apical changeHealthy tooth a. Incipient acute apical periodontitis b. Advanced ’’ ’’ ’’ (i) acute periapical abscess (ii) recrudescent / phoenix abscess (iii) subacute periapical abscess
  • Abscess Healthy tooth Early apical change
  • Abscess Tooth becomes extremely tender Vascular congestion Regional anoxia Cell breakdown(autolysis) Neutrophils increase in number Release osteolytic fragments Pus core
  • Gumboil (parulis) Breach the cortical bone (sinus opening) “STOMA” ACUTE CHRONIC
  • parulis / gum boil (acute/chronic) stoma (chronic)
  • Apical periodontitis
  • A draining sinus is evident on the labial aspect of the upper left lateral incisor. (A) A gutta percha (GP) point has been placed into the draining sinus in order to trace its origin. (B) The radiograph taken with the GP point in the sinus shows that it tracks from the periapical region of the upper left central incisor, which has a chronic apical abscess. The lateral incisor has chronic apical periodontitis but this tooth is not associated with the draining sinus.
  •  Toxic components from pulp irritants / necrosis  Occlusal disharmony – persistant periapical tissue compression  Related to root canal procedures ETIOLOGY of Painful pulpoperiapical pathoses
  • Etiologic factors related to rot canal procedures Note the space between the gutta-percha filling and the root canal walls clearly visible JOSE´ F. SIQUEIRA
  • Common problems that may cause post-treatment disease at least seven problems 1. Inadequate RCT without iatrogenically altered root canal morphology 2. Inadequate RCT with iatrogenically altered root canal morphology 3. Infection remaining in inaccessible areas in the apical portion of the root 4. Extraradicular infection including extruded dentin debris with bacteria present in the dentinal tubules 5. True radicular cysts and tumors 6. Foreign body reaction to cholesterol crystals or extruded materials such as talc- contaminated guttapercha, particles of paper points, and particles of sealer 7. Vertical root fractures
  • The quality of the root canal obturation as visualized on a buccal–lingual radiograph is in no way indicative that the root canal was well sealed, particularly when canals are oval or ribbon-shaped in transverse section. Note the discrepancy of the image taken in a buccal–lingual direction as compared to that taken in a mesio-distal direction. Endodontic Topics 2005, 10, 123–147
  • Diagnosis  Slight tenderness to intense continuous throbbing pain  Sense of fullness  Readily localised – tenderness on percussion  Palpable fluctuant swelling  Vitality test (if viable Cfibers )  Radiographs
  • 2 . Non-Painful pulpoperiapical pathoses a. Pulpopariapical osteosclerosis(condensing osteitis) b. Incipient chronic apical periodontitis c. Advanced ’’ ’’ ’’ (i) periapical granuloma (ii) chronic periapical abscess (iii) periapical cyst
  • 2 . Non-Painful pulpoperiapical pathoses a. Pulpopariapical osteosclerosis(condensing osteitis) b. Incipient chronic apical periodontitis c. Advanced ’’ ’’ ’’ (i) periapical granuloma (ii) chronic periapical abscess (iii) periapical cyst
  • Pulpoperiapical osteosclerosis (Condensing osteitis) Occur most frequently in the mandible, around teeth with a periapical granuloma or radicular cyst, RCT,or restorations. exudate from the pulp (low toxicity and long standing) the resulting mild irritation circumscribed proliferation of the periapical bone. “condensing osteitis or focal sclerosing osteomyelitis”
  • Incipient Chronic apical periodontitis Initially chronic periapical connective response to pulpal irritants characterized by :  slightly widened apical periodontal space (containing dilated blood vessels, a mild inflammatory exudate)  a dense accumulation of chronic inflammatory cells(plasma cells and lymphocytes) If the pulpal contaminants are not removed the response will intensify to one of the acute or chronic forms
  • a. Pulpopariapical osteosclerosis(condensing osteitis) b. Incipient chronic apical periodontitis c. Advanced ’’ ’’ ’’ (i) periapical granuloma (ii) chronic periapical abscess (iii) periapical cyst
  • Periapical granuloma This is advanced form of chronic apical periodontitis; characterized by growth of granulation tissue and the presence of chronic inflammatory cells (granulomatous) in response to continued pulpal irritation.
  • Zones of periapical granuloma Exudative Granulomatous Granulofibrotic Fibrotic granulomas O3 OR,Endo 1996:81:93-102
  • Periapical cyst “A periapical cyst is chronic inflammatory response of the periapex that develops from chronic lesions with preexisting granulomatous tissue.” characterized by: Central fluid filled epithelium lined cavity surrounded by granulomatous tissue and peripheral fibrous encapsulation.
  • Periapical / Radicular cyst  Direct sequel to chronic AP  Incidence: 6-55%  Two types : true and pocket  Typical radiographic appearance-round/pear shaped radiolucent unilocular lesion less than 1cm in diameter  Process of formation Dormant cell rests of malassez proliferate Epithelium lined cavity comes into existence Cyst grows in size
  • Do periapical cysts heal ?
  • Differential diagnosis
  • Granuloma vs Cyst vs Abscess Chronic non painful Definite outline Smaller in size Chronic non painful Sclerotic opaque border Bigger in size Contain more protein and albumins Acute /Chronic Pain/non painful Swelling/parulis Sinus opening(chronic) Diffuse outline Mobility of the tooth history Conformative  histology
  • Condensing osteitis Hypercementosis …. Vital , lying within intact lamina dura and PDL space Periapical cemental dysplasia ….lesion is seperated from the surrounding normal bone by a radioluscent border , vital Osteosclerosis …. idiopathic
  • Odontogenic pain Dentinal hypersensitivity Reversible pulpitis Irreversible pulpitis Acute apical periodontitis Acute apical abscess
  • Non odontogenic pain –musculoskeletal Myofacial pain TMD bruxism Non odontogenic pain– neuropathic Trigeminal neuralgia Atypical odontalgia Glossopharyng neuralgia Non odontogenic pain– neurovascular migraine cluster headache Non odontogenic pain – inflammatory allergic rhinitis bacterial sinusitis Non odontogenic pain – systemic disorders Cardiac pain Herpes zoster Sickle cell anaemia Neoplastic disease
  • Ludwig’s angina  “potentially life-threatening, rapidly expanding, diffuse inflammation of the submandibular and sublingual spaces that occurs most often in young adults with dental infections.” Symptoms:  severe neck pain  Swelling  Fever  Malaise  Dysphagia Stridor suggests an impending airway crisis. Causative bacteria include many gram-negative and anaerobic organisms, streptococci and staphylococci
  • Ludwig’s angina The submandibular space is composed of two spaces separated anteriorly by the mylohyoid muscle: the sublingual space, which is superior, and the submaxillary space, which is inferior. The spread of infection is halted anteriorly by the mandible and inferiorly by the mylohyoid muscle. The infectious process expands superiorly and posteriorly, elevating the floor of the mouth and the tongue. The hyoid bone limits the process inferiorly, and swelling spreads to the anterior aspect of the neck, causing distortion and a "bull neck" appearance. This then evolves to
  • Cellulitis (Phlegmon)  Cellulitis is a diffuse inflammation of the soft tissues which is not circumscribed or confined to one area,but which,in contradistinction to the abscess,tends to spread through tissue spaces along facial planes.
  • Cellulitis –etiology (of face and neck)  Dental infection as a sequelae of an abscess or osteomyelitis,or following periodontal infection.  Pericoronitis (operculitis)  Infection following tooth extraction ( injection either thro an infected needle or infected area)
  • Cellulitis -pathogenesis Microorganisms Hyaluronidase / fibrinolysins Breakdown or dissolve intercellular cement substance (hyaluronic acid and fibrin) Streptococci are particularly potent producers of hyaluronidase Staphylococci – less potent – also pathogenic – freq give rise to cellulitis
  • Cellulitis – clinical features (of face and neck)  Painful swelling of the involved soft tissues  Skin overlying is firm and brawny,inflamed,sometimes even purplish (when spread is in deeper planes –normal)  Moderatily ill-elevated temperature  Leukocytosis  Regional lymphadenitis Infections arising in the maxilla – perforate the outer cortical layer of bone above buccinator attachment –swelling of upper half of face In mandible –below buccinatorattachment – lower half of face Treatment – analgesics + antibiotics + removal of cause
  • Osteomyelitis If the periapical infection and inflammation extend through the marrow spaces of the jaw, the result is osteomyelitis.  Odontogenic infection  Infection thro PDL space  Extraction wound  Trauma-fracture  Metastasis from remote area of infection In this case, you can identify the offending tooth causing the diffuse and irregular bone destructio
  • Osteomyelitis – predisposing conditions  Malnutrition  Diabetes  h/o Alchoholism  Leukemia  Various anaemias  Conditions that are characterized by the formation of avascular bone that precludes an effective defensive response • Osteopetrosis • Paget’s disease • Florid osseous dysplasia • Post-irradiation states • Flourosis
  • Classification - Osteomyelitis  Suppurative > acute suppurative > chronic suppurative * primary * secondary > infantile  Non suppurative > diffuse sclerosing > focal sclerosing > proliferative periosteitis > osteoradionecrosis
  • Acute osteomyelitis  Develops in a matter of days  Does not show any early radiographic changes  Most commonly arises from a periapical abscess  Ther is no swelling or redness until later-penetrated cortex and involved periosteum  WBC count and Temp  Reflex spasm of muscles attached to the involved area of bone  Local signs and symptoms: severe pain,soreness of the involved teeth,which are also loose,regional lymphadenopathy,parasthesia/anaesthesia of lip. Radiograph – solitary/multiple small radioluscent areas Trabeculae-decreased density,outlines become blurred or fuzzy.
  • Acute suppurative osteomyelitis The clinical manifestations in this case are severe and debilitating. Radiograph- Almost the entire body of the mandible is involved and shows diffuse mottled resorption. The decayed first molar is the guilty tooth.
  • Chronic osteomyelitis  is persistent abscess of bone charact by inflammatory processes , including necrosis of mineralised and marrow tissues,suppuration,resorption,sclerosis, and hyperplasia. o Symptoms are milder, o pain is less , o bone destruction is slower, o sinus tracts develop intermittently and then cease draining and close.
  • Chronic sclerosing osteomyelitis Here is an extensive chronic osteomyelitis characterized by bone formation only (chronic diffuse sclerosing osteomyelitis).
  • Garres osteomyelitis(COPP)  Children/young adults  Mandibular molars-inferior border of mandible  Hard bony nontender swelling  Size:1-2cm;cortex becomes 2-3cm thick  R/f: onion skin appearance-alt radioluscent,opaque layers
  • Sequestrum In many cases of osteomyelitis there are bone sequestra. This necrotic piece of bone is being actively resorbed and is surrounded by intense inflammation and granulation tissue.
  • Treatment guideline for acute or chronic osteomyelitis  Disrupt the infectious foci.  Debride any foreign bodies necrotic tissue, or sequestra.  Culture and identify specific pathogens for eventual definitive antibiotic treatment.  Drain and irrigate the region.  Begin empiric antibiotics based on Gram stain.  Stabilize calcified tissue regionally.  Consider adjunctive treatments to enhance microvascular reperfusion (usually reserved for refractory forms only).  Trephination  Decortication;sequestrectomy  Vascular flaps  Hyperbaric oxygen therapy  Reconstruction as necessary following resolution of the infection.
  • Extra radicular infections Found in following situations: 1. Acute apical periodontitis lesions 2. Periapical actinomycosis 3. In ass with pieces of infected root dentin that may be displaced into the periapex during RC instrumentation or have been cut off from the rest of root by massive apical resorption 4. Infected periapical cysts, particularly in periapical pocket cysts with cavities open to the root canal.
  • Actinomycosis is a chronic, granulomatous, infectious disease in humans and animals caused by the genera Actinomyces and Propionibacterium (McGhee et al.1982). Etiological agent :  Actinomyces bovis- first species to be identified(Harz 1879).  in cattle - ‘lumpy jaw’ or ‘big head disease’  characterized by>extensive bone rarefaction, >swelling of the jaw, >suppuration > fistulation. Actinomycosis Causative agents  nonacid fast, non-motile, Gram-positive ‘sulphur granules’ - yellow specks in exudates. a ‘starburst appearance’ ‘ray fungus’.
  • Actinomycosis Human actinomycosis is clinically divided into  Cervicofacial(60%)  Thoracic(15%)  Abdominal forms(20%) (Kapsimalis &Garrington 1968, Oppenheimer et al. 1978). The most common species isolated from humans is A. israelii which is followed by Propionibacterium propionicum (Buchanan & Pine 1962) (Wolff & Israel 1891), Actinomyces naeslundii (Thompson & Lovestedt 1951), Actinomyces viscosus and Actinomyces odontolyticus in descending order (Batty 1958)
  • Foreign body reactions  Oral pulse granuloma  Cellulose granuloma  Gutta percha  Other materials- amalgam,endo sealants, and calcium salts derived from periapically extruded Ca(OH)2
  • CONCLUSION It is essential that we understand the progressive nature of the periapical disease process as well as how and why the various stages occur so they can be diagnosed and managed appropriately.
  • Thank you