diseases of pulp and periapical tissues

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Pulpitis is an inflammation of pulp tissue, a response to surrounding environment The vitality of the tooth depends on defence response of pulp dentine complex by: - Sclerotic dentin - Tertiary dentin - Calcified bridge of dentinal tubules



MECHANICAL: Trauma, iatrogenic damage and barometric changes. THERMAL: uninsulated metallic restorations and dental procedures like cavity preparation, exothermic chemical reactions of dental materials etc. CHEMICAL: Irritation from certain dental materials or from erosion. BACTERIAL: Through toxins or from direct extension of caries



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Severity and duration of irritant. Nature of irritant. Health condition of the pulp or pre-existing state of the pulp Apical blood flow Local anatomy of the pulp chamber Host defence



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I. According to pathological condition: - - Focal or acute reversible pulpitis (Pulp hyperaemia) - Irreversible pulpitis II. According to its duration: - - Acute pulpitis - Chronic pulpitis III. According to presence of dentin covering the pulp chamber: - - Open pulpitis - Closed pulpitis

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IV. According to extension of inflammation in pulp tissue: - - Partial pulpitis - Complete / total pulpitis V. According to amount of pus formation: - - Exudative pulpitis - Suppurative pulpitis

ACUTE REVERSIBLE PULPITIS(Focal reversible pulpitis, Pulp hyperaemia) : 

ACUTE REVERSIBLE PULPITIS(Focal reversible pulpitis, Pulp hyperaemia)

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Acute reversible inflammation of pulp tissue characterized by vascular dilatation AETIOLOGY: - Any mild irritants

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CLINICAL FEATURES: - Signs and symptoms: painful Duration: 10-15 minutes, severe and short Precipitating factors of pain: hot and cold agents Nature of pain: Throbbing, continuous and radiating. Pain stops when precipitating factors are removed

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The pain depends on - The size of exposed pulp (size of dental caries) Severity of pulp inflammation Age of patient Nature of covering dentine

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HISTOLOGICAL FEATURES: - Inflamed pulp tissue contains dilated blood vessels of various sizes and are lined by endothelial cells Presence of normal odontoblasts indicate vitality of the pulp tissue.

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PROGNOSIS-: It is a reversible condition. If it is treated , pulp will return back to its normal status. If it is left untreated , it will not return back to its normal status but it will enter the next phase....



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CLINICAL FEATURES: - Duration : - more than 10-15 minutes, severe and continuous, especially at night Precipitating factors of pain : - spontaneously as well as hot and cold agents Nature of pain : - Throbbing continuous and radiating pain The pain does not stop even when precipitating factors are removed.

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PROGNOSIS: - If it is left untreated, it will change to chronic pulpitis or pulp necrosis



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It is a chronic inflammation of pulp tissue characterized by specific clinical features. CLINICAL FEATURES: - Signs and symptoms: - painful Duration: - long duration (few days to months).

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Precipitating factors of pain: - hot, cold agents and during biting. Nature of pain: - Mild and intermittent pain The pain stops when precipitating factors are relieved and when the tooth is treated

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The pain depends on: - The size of exposed pulp (size of dental caries) Severity of pulp inflammation Age of patient Nature of covering dentin


HISTOPATHOLOGICAL FEATURES: - The pulp tissue contains dilated blood vessels with varying sizes. Degenerated odontoblasts seen. Areas of chronic inflammatory cells and fibrosis can be seen around inflamed areas

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PROGNOSIS: - It is dependant on the success of pulp capping.



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It is a chronic inflammation of pulp tissue characterized by hyperplasia of connective tissue of pulp in the form of polypoid mass which originates from exposed pulp chamber

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CLINICAL FEATURES : - Site: A grossly carious molar (permanent/deciduous) where pulp chambers are wide, having multiple roots with highly vascular pulp tissue Shape : nodular fungated mass fills pulp chamber

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Size : variable Colour : reddish, bleeds readily Covering surface : intact or ulcerated


HISTOLOGICAL FEATURES: - Mass consists of proliferation of granulation tissue with newly formed, dilated blood vessels of varying sizes, chronic inflammatory cells and fibrosis Generalized degenerated odontoblasts also called “Wheat Shafing” of Odontoblasts The mass is covered by hyperplastic stratified squamous epithelial surface Source of epithelial cells are from saliva or desquamated mucosa of cheeks or gingiva

PULP CALCIFICATION (Pulp Stone or Denticles) : 

PULP CALCIFICATION (Pulp Stone or Denticles)

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It is a localized / generalized condition of pulp tissue characterized by formation of pulp stone in the form of calcified bodies CLINICAL FEATURES : - Site: coronal or radicular pulp Size: variable Signs and symptoms : painless

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RADIOGRAPHIC FEATURES: - Radiopaque mass / masses with variable sizes inside the pulp chamber or pulp canals.

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HISTOLOGICAL TYPES: - True pulp stone - consists of dentinal tubules. False pulp stone - consists of concentric calcified rings Free pulp stone - is freely located within the pulp tissue Attached pulp stone - is adherent to dentin wall Embedded pulp stone - is surrounded by secondary dentin

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COMPLICATIONS: - It interferes with root canal treatment. Can cause pain if it impinges on major pulp nerves.



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It is an irreversible condition of pulp tissue characterized by dead pulp tissue and degeneration ( necrosis ) AETIOLOGY : -Severely irritant agents. CLINICAL FEATURES : - Signs and symptoms : painful Duration : 10-15 minutes, severe and short

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Precipitating factors of pain: hot and cold agents Nature of pain: Throbbing, continuous and radiating. The pain stops when precipitating factors are relieved.



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It refers to a mass of chronically inflamed granulation tissue at the apex of a non vital tooth. May arise either after an acute condition like periapical abscess becomes quiet or it may arise de novo. Important – these lesions are not static and may transform into periapical cysts or undergo acute exacerbation.

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CLINICAL FEATURES: - Mostly asymptomatic. Pain & sensitivity can develop if acute exacerbation occurs. No mobility or sensitivity to percussion of involved tooth. Pulp vitality tests are negative.

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RADIOGRAPHIC FEATURES: - Lesion can be either well / ill defined. Variable sized from small to large. Loss of apical lamina dura. Root resorption is common. Cannot distinguish periapical granulomas from periapical cysts on a radiograph.

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HISTOLOGICAL FEATURES:- Lesion shows inflamed granulation tissue containing a dense lymphocytic infiltrate mixed with PMNL’s, plasma cells and macrophages. Epithelial rests of Malassez may be seen within the granulation tissue.

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Cholesterol clefts may also be seen along with associated multinucleated giant cells. Areas of extravasation of RBC’s and hemosiderin pigmentation is also common.

RADICULAR CYST(Peripaical cyst / Apical periodontal cyst) : 

RADICULAR CYST(Peripaical cyst / Apical periodontal cyst)

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By definition, a radicular cyst arises from epithelial rests of Malassez located in the PDL as a result of inflammation. Often, radicular cyst remains behind in jaws after removal of infected tooth – then called RESIDUAL CYST.

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CLINICAL FEATURES: - Age incidence: peak in 3rd, 4th and 5th decades. Sex incidence: Slightly more in males. Site predilection: Maxillary anterior region. Frequency: Commonest cystic lesion of jaws.

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Signs & symptoms: Primarily symptom less. Discovered accidentally during routine dental X ray exam.

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Slowly enlarging hard bony swelling initially. Later, if cysts breaks through cortical plates, lesion becomes fluctuant. Diagnostic criteria – associated teeth are non vital Rare in deciduous teeth.

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RADIOLOGICAL FEATURES: Classically presents as round / ovoid radiolucency with sclerotic borders and associated with pulpally affected tooth / teeth. If infection supervenes, the margins become indistinct, making it impossible to distinguish it from a periapical granuloma.

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DIFFERENTIAL DIAGNOSIS: - Following lesions must be distinguished from other periapical radiolucencies– 1. Periapical granuloma 2. Peripaical cemento – osseous dysplasia (early lesions)

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PATHOGENESIS: - 1. PHASE OF INITIATION: Accepted generally that rests of Malassez included within a developing periapical granuloma proliferates to form the lining of radicular cyst. How these cells are stimulated is not clear. Some product of non vital pulp can be responsible which simultaneously evokes an inflammatory response in CT. Immune factors also held responsible as plenty of plasma cells are seen in a periapical granuloma.

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2.PHASE OF CYST FORMATION: Can occur in two possible ways. One theory states that epithelium proliferates and covers the bare CT surface of the abscess cavity. Another theory – cyst cavity forms within proliferating epithelium as the cells in center move away from their nutrient source. Prepared by Dr Sundeep S Bhagwath

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3. PHASE OF ENLARGEMENT: - Enlargement occurs by collection of fluid within the lumen of the cyst. Osmosis plays an important role here as the cyst wall appears to have the properties of a semi permeable membrane.

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HISTOLOGICAL FEATURES:- Lined partly / completely by non keratinized epithelium of varying thickness. Epithelium usually shows arcading around the CT. The CT wall shows inflammatory infiltrate mainly in the form of lymphocytes and plasma cells.

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Hyaline / Rushton bodies are found in epithelium and rarely in CT wall. These are curved or linear structures with eosinophilic staining properties.

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Cholesterol crystals in from of clefts are often seen in the CT wall, inciting a foreign body giant cell reaction. Originate from disintegrating RBC’s in presence of inflammation. Different types of dystrophic calcification are also seen in CT wall.

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Mucus cell metaplasia as well as respiratory cells may be seen in the epithelial lining. Keratinization if found is due to metaplasia and must not be confused with an OKC.

PERIAPICAL ABSCESS(Acute dentoalveolar abscess) : 

PERIAPICAL ABSCESS(Acute dentoalveolar abscess)

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Collection of acute inflammatory cells at the apex of a non vital tooth is called periapical abscess. Acute lesions may arise either as in initial pathosis or as an acute exacerbation of a chronic periapical pathology (Phoenix abscess).

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CLINICAL FEATURES:- Initial stages – tenderness of affected tooth. Later – pain becomes intense, with extreme sensitivity to percussion. Extrusion of tooth in its socket. Systemic findings – fever, malaise, chills.

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Abscess may spread along path of least resistance through medullary spaces resulting in Osteomyelitis. Can also perforate cortical bone and spread to soft tissues – Cellulitis. It can also drain through an intraoral sinus tract. Opening of such a tract is usually covered by a granulation tissue – Parulis.

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Periapical abscesses may also channelize through the overlying skin and drain via a Cutaneous sinus. If an abscess begins to drain, it becomes asymptomatic due to lack of collection of pus within the cavity.

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RADIOGRAPHIC FEATURES: - In initial stages – thickening of periodontal ligaments. Later – ill defined radiolucency.

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HISTOLOGICAL FEATURES: - Microscopic sections are not usually made as specimen is fluid. Abscess contains abundant PMNL’s mixed with inflammatory exudate, cellular debris and histiocytes. Phoenix abscesses may also contain soft tissue component comprising of granulation tissue mixed with areas of abscess



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It is a rapidly spreading inflammation of the soft tissues characterized by diffuse pus formation. This happens if an abscess is not able to establish drainage through the skin surface or into oral cavity.

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TYPES: - Cellulitis arising from dental infection and spreading through soft tissues of head and neck can take various forms. Mostly, infection spreads through tissue spaces like canine space, infratemporal space, pharyngeal space, buccal space, submental and submandibular space etc.

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Two especially dangerous forms of cellulitis are – - Ludwig’s angina - Cavernous sinus thrombosis

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Canine space infection Infection involving multiple spaces


LUDWIG’S ANGINA Cellulitis of submandibular region involving sublingual, submandibular and submental spaces. In 70% cases develops from spread of infection from mandibular teeth. Increased prevalence in immunocompromised patients like AIDS, aplastic anemia, organ transplantation etc.

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CLINICAL FEATURES: - After reaching submandibular region, infection extends to lateral pharyngeal and retropharyngeal spaces. LA causes massive swelling of neck extending close to clavicles. There is posterior enlargement and protrusion of tongue. Pain in neck and floor of mouth.

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Other symptoms – dysphagia, dysphonia, drooling and sore throat. Lateral pharyngeal space involvement may cause respiratory obstruction due to laryngeal edema. In sever cases – tachypnea, dyspnea, tachycardia, stridor may also be noted. General signs – fever, malaise, leukocytosis, and raised ESR.


CAVERNOUS SINUS THROMBOSIS Occurs when infection from maxillary premolars / molars perforates buccal cortical plate and enters maxillary sinus, pterygopalatine space or infratemporal space and reaches the orbit. From here, infection enters cavernous sinus through cranial vault.

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CLINICAL FEATURES: - Periorbital edema including lateral border of nose, protrusion and fixation of eyeball. Pupil dilatation, lacrimation, photophobia and loss of vision may also occur. Pain along distribution of ophthalmic and maxillary branches of Vth cranial nerve. Proptosis, chemosis and ptosis seen in 90% cases. Fever, chills, headache, sweating, tachycardia, nausea and vomiting also occur.



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Refers to acute / chronic inflammatory process in medullary spaces or cortical surfaces of bones. Various patterns recognized like focal and diffuse sclerosing, proliferative periostitis etc.

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TYPES OF OSTEOMYELITIS: - Acute osteomyelitis Chronic osteomyelitis Diffuse sclerosing osteomyelitis Condensing osteitis (Focal sclerosing osteomyelitis) Osteomyelitis with proliferative periostitis. Alveolar osteitis

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PREDISPOSING FACTORS: - After odontogenic infections Trauma to jaws Presence of ANUG Chronic systemic diseases Immunocompromised states Tobacco and alcohol abuse Diabetes mellitus Exanthematous fevers Malignancy Malnutrition


ACUTE OSTEOMYELITIS Acute osteomyelitis occurs when acute inflammation spreads through medullary spaces of bone. CLINICAL FEATURES: - Age incidence: Any age Sex incidence: Strong male predilection Site predilection: Mostly in mandible. Maxilla is involved primarily in children.

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Signs & symptoms: Fever, leukocytosis, lymphadenopathy and soft tissue swelling of affected area. X-rays can show an ill defined radiolucency. Occasionally, fragments of necrotic bone can be seen separating from surrounding normal bone – Sequestrum. If sequestrum is surrounded by vital bone – Involucrum.

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HISTOLOGICAL FEATURES: - Biopsy specimen usually contains necrotic bone, showing loss of osteocytes from lacunae and bacterial colonization. Bone periphery shows necrotic debris and infiltration with PMNL’s. Specimen diagnosed as sequestrum unless there is good clinico-pathologic correlation.


CHRONIC OSTEOMYELITIS It can arise either de novo from the onset or as a continuation of acute osteomyelitis, if it is not resolved quickly. CLINICAL FEATURES: - Age incidence: Any age Sex incidence: Strong male predilection Site predilection: Mostly in mandible.

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Signs & symptoms: Pain, swelling, purulent discharge, sinus formation, sequestrum formation, tooth loss. Frequent acute exacerbations may occur if infection continues for a long time. X-rays reveal ill defined, moth eaten radiolucency often showing a central radiopacity (sequestrum).

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HISTOLOGICAL FEATURES: Biopsy material contains significant soft tissue component consisting of chronically inflamed fibrous CT filling intertrabecular areas of bone. Scattered areas of sequestrum may also be noted.


DIFFUSE SCLEROSING OSTEOMYELITIS Characterized by pain, inflammation, varying degrees of periosteal hyperplasia, sclerosis and radiolucency of affected bone. Can be confused clinically and radiologically with certain other intrabony pathoses like florid cemento-osseous dysplasia or Paget's disease of bone etc.

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CLINICAL FEATURES: - Age incidence: Almost exclusively in adults. Sex incidence: Nil Site predilection: Primarily in mandible Signs & symptoms: Pain and swelling are uncommon. To make a definitive diagnosis of diffuse sclerosing osteomyelitis, microbiological cultures must be positive.

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RADIOGRAPHIC FEATURES: - Increased radiopacity around sites of chronic inflammation like periodontitis, pericoronitis, periapical pathology etc. Sclerosis occurs more in alveolar crest regions of tooth bearing areas.

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HISTOLOGICAL FEATURES:- Sclerosis and remodeling of bone. Significant inflammation of bone is not seen even though sclerosis occurs adjacent to inflammation. Necrosis of sclerotic bone secondary to inflammation may occur. In this case, necrotic bone separates and is surrounded by granulation tissue


FOCAL SCLEROSING OSTEOMYELITIS(Condensing osteitis) This refers to a focal area of bone sclerosis associated with apices of pulpally involved (caries, deep restorations or pulp necrosis) teeth. To be diagnosed as condensing osteitis, association with inflammation is essential, as it resembles several other intrabony pathoses.

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CLINICAL FEATURES: - Occurs mostly in children and young adults. Mostly occurs in mandibular premolar/molar area, associated with pulpitis / pulp necrosis. Localized, uniform zone of increased radiopacity seen adjacent to tooth apex. No swelling / cortical expansion noted clinically.

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DIFFERENTIAL DIAGNOSIS: - This lesion must be distinguished from Focal cemento osseous dysplasia – it shows a radiolucent border. Idiopathic osteosclerosis – here, the lesion is separated from the tooth apex.


OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS Also called Periostitis ossificans or Garrѐ’s Osteomyelitis. It is a type of osteomyelitis associated with periosteal bone formation.

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CLINICAL FEATURES: - Age incidence: Children & young adults Sex incidence: Nil Site predilection: Mostly in premolar/ molar regions of mandible.

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Signs & symptoms: Swelling may be noted on lower border of mandible. Pain may / may not be present. Radiographs demonstrate radiopaque laminations roughly parallel to each other and the underlying cortical surface (onion skin appearance).

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HISTOLOGICAL FEATURES: Shows parallel rows of higly cellular, woven bone in which the individual trabeculae are oriented perpendicular to surface. Sometimes, trabeculae are interconnected or they may be scattered, resembling fibrous dysplasia. In between trabeculae, fibrous CT is relatively non inflamed.

ALVEOLAR OSTEITIS(Dry socket / Fibrinolytic alveolitis) : 

ALVEOLAR OSTEITIS(Dry socket / Fibrinolytic alveolitis) Sometimes, the blood clot at the extraction site fails to organize which eventually leads to delayed healing and causes a condition called “Dry socket”. Research shows it is due to transformation of plasminogen to plasmin with resultant lysis of fibrin and formation of kinin (pain mediators).

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PREDISPOSING FACTORS: - Local trauma Estrogens Bacterial toxins Inadequate irrigation of surgery site Tobacco abuse.

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CLINICAL FEATURES: - Age incidence: Between 20 – 40 years Sex incidence: Nil Site predilection: Posterior mandibular teeth, especially impacted third molars.

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Signs & symptoms: Affected extraction site filled with a dirty gray clot, which is lost, leaving behind a bare, bony socket (Dry socket). Diagnosis is confirmed by probing of socket which shows an exposed and extremely sensitive bone. Severe pain, foul smell and lymphadenopathy develop within 3 – 4 days of extraction.


BIBLIOGRAPHY Soames JV, Southam JC. Oral pathology/. 3rd ed. Oxford 2002. Shafer WG, Hine MK, Levy BM. A text book of oral pathology. 6th ed. W.B. Saunders Company. Phil, London, Toronto, 2005. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2nd ed. WB Saunders Company. Phil, London, Toronto, 2007. Cawson RA, Odell EW, Porter S. Cawson’s essentials of oral pathology and oral medicine, 7th Ed, Churchill Livingstone, 2002. Regezi JA, Sciubba JJ, Jordan RCK. Oral pathology: Clinical Pathologic Correlations. 4th ed. Saunders Company, 2003.


ACKNOWLEDGEMENT All pictures in this presentation are courtesy of the authors mentioned in the bibliography.

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