InflammationDr. Amit T. Suryawanshi

Oral and Maxillofacial Surgeon Pune, India

Contact details :Email ID - amitsuryawanshi999@gmail.comMobile No - 9405622455

Contents

• Introduction. • Definition.• Historical background.• Cardinal signs of inflammation.• Types of inflammation.• Pathophysiology of inflammation.• Inflammatory cells & mediators.• Clinical perspectives. • Conclusion. • References.

Introduction

• Survival of all living organisms requires that they should eliminate foreign invaders , such as infectious pathogens & damaged tissues .

These functions are mediated by complex host immune response called as an Inflammation.

Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process.

Hence without inflammation, wounds and infections would never heal.

Inflammation

• Definition –

The word inflammation is derived from

Latin word inflammare, which means “to set

on fire.”

Inflammation

Inflammation is defined as “a protective response intended to eliminate the original cause of cell injury , necrotic tissues and tissues resulting from original insult . ”

Terms ending with suffix “ itis” denote inflammation .

Historical Background

1. Word inflammation – Latin word inflammare ( meaning – to set on fire ) 2. Celsus – A roman physician and medical writer (30

BC to 45 AD ) gave 4 cardinal signs of inflammation saying

“ Rubor et tumor cum calore et dolore.” (meaning - Redness and swelling come with heat

and pain )

3. Virchow added 5th Cardinal sign of inflammation in 1871

i.e. functio laesa (loss of function)

4. Cohnheim gave First description of diapedesis in 1873.

5. Lewis described Inflammation as the ‘‘triple response’’ to injury in 1927

Cardinal Signs Physiological rationale

1. Rubor ( Redness) Increased Blood flow

2. Tumor (Swelling ) Exudation of fluid

3. Calor (Heat) Increased Blood flow , Exudation of fluid, Release of inflammatory mediators

4. Dolor ( Pain ) Stretching of pain receptors and nerves by inflammatory exudates , chemical mediators

5. Functio laesa (Loss of function)

Pain,Disruption of tissue structure,Fibroplasia and metaplasia

Cardinal signs of inflammation & Its Physiological rationale

1. Acute inflammation – It is the rapid response to the injury or microbes or

other foreign substances that is designed to deliver leukocytes & plasma proteins to the site of injury .

Causes –2. Infections – Bacterial , viral , fungal or parasitic3. Trauma –Blunt or Penetrating 4. Tissue necrosis- 5. Foreign bodies – sutures 6. Immune reactions

Types of inflammation

• Outcomes of acute inflammation-1. Resolution2. Progression to chronic inflammion.3. Scarring or fibrosis

2. Chronic inflammation – It is inflammation of prolonged duration in which

active inflammation, tissue injury & healing proceed simultaneously .

Causes –1. Persistent infection 2. Immune mediated inflammatory diseases3. Prolonged exposure to potentially toxic agents

• Outcomes of Chronic inflammation-

1. Resolution2. Scarring or fibrosis

Pathophysiology of inflammation

Inflammed (Vasodilation in capillary bed)

NormalArteriole Venule

Capillary bed

Leukocyte Transmigration , Chemotaxis & Phagocytosis

Resolution of Inflammation

Pathophysiology of inflammation

Inflammatory cells

1. Blood leukocytes – Neutrophils , Macrophages, Lymphocytes.2. Plasma cells 3. Connective tissue cells – Fibroblasts, Mast cells.4. Cells of vascular walls .

Inflammatory mediators • Definition – Chemical substances that trigger certain

processes in an inflammatory reaction.

Cell derived Plasma derived

Histamine Kinin system mediators

Serotonin C- reactive protein

Neutrophilic proteases Complement system mediators

Interleukins( IL-1 . TNF- α )

Chemokines

Arachidonic acid (PG, LT)

PAF

• Plasma proteins & extracellular matrix also play an important role in process of inflammation.

Differences between Acute & Chronic Inflammation

Acute inflammation Chronic inflammation

Definition It is the rapid response to the injury or microbes or other foreign substances that is designed to deliver leukocytes & plasma proteins to the site of injury .

It is inflammation of prolonged duration in which active inflammation, tissue injury & healing proceed simultaneously .

Onset Rapid Insidious

Duration Short ( Few minutes to days )

Long (Days to years )

Acute inflammation Chronic inflammation

Specificity Non- specific Specific, where immune response is activated

Cells involved Neutrophils Lymphocytes , plasma cells , macrophages , fibroblasts

Vascular changes

Active vasodilation ,Increased vascular permeabilty

New vessels formation(Neoangiogenesis )

Fluid exudation & edema

Present Absent

Cardinal signs Present Absent

Acute inflammation

Chronic inflammation

Tissue necrosis Absent Ongoing

Systemic manifestations

High grade fever Low grade fever, weight loss , anemia

Clinical Perspectives

Inflammatory diseasesAcute inflammatory diseases-

Chronic inflammatory diseases -

1. Acute suppurative osteomyelitis

1. Chronic suppurative osteomyelitis

2. Chronic focal sclerosing osteomyelitis

3. Chronic diffuse sclerosing osteomyelitis.

4. Garre’s osteomyelitis

Acute inflammatory diseases-

Chronic inflammatory diseases -

Acute Pericoronitis Chronic Pericoronitis

Acute Sialadentitis Chronic Sialadentitis

Acute Maxillary sinusitis Chronic Maxillary sinusitis

Acute Stomatitis Chronic Stomatitis

Infectious arthritis _

_ Rheumatoid arthritis

Rheumatoid arthritis

• Etiology –

1. Unknown 2. The is evidence that it may be a hypersensitive reaction to bacterial toxins specifically of streptococci.

It is a debilitating systemic disease of unknown origin , characterized by progressive involvement of the TM joint ,(particularly bilateral involvement)

Clinical features –General – 1. Slight fever, Weight loss, Fatigue Extraoral – 1. Swelling over joint region , Stiffness , pain on movement . 2. Clicking is uncommon. 3. Over period of years there may be ankylosis but its not inevitable.

• Radiographic appearance -

Infectious Arthritis

• Incidence- very rare.

• Etiology –

Infection – Gonococci, Streptococci, staphylococci, pneumococci & tubercle bacillus .

• Etiopathogenesis – 1. Spread can be hematogenous , Lymphatic

or by direct extension of foci of infection . 2. Most commonly , it spreads directly from foci of infection. - Adjacent cellulitis - Osteomyelitis Which may follow - Dental infection. - Infection of parotid gland, ear.

• Clinical features – 1. Severe pain in joint , tender on palpation in joint region. 2. Trismus. 3. Results in ankylosis , most commonly fibrous ankylosis .

Osteomyelitis • Definition – It is defined as an inflammation of marrow

spaces of bone with tendency of involvement of cortical plates and periosteum.

• Etiology – 1. Dental infection

Predisposing factors –2. Fractures 3. Gunshot wounds 4. Radiation damage 5. Paget's disease6. osteopetrosis

• Systemic factors –1. Malnutrition 2. Acute leukemia3. Uncontrolled diabetes mellitus 4. Sickle cell anemia5. Chronic alcoholism

Types of osteomyelitis –

1. Acute suppurative osteomyelitis 2. Chronic suppurative osteomyelitis 3. Chronic focal sclerosing osteomyelitis4. Chronic diffuse sclerosing osteomyelitis.5. Garre’s osteomyelitis

Acute suppurative osteomyelitis

• Definition-• “Acute suppurative osteomyelitis of jaw is a

sequela of periapical infection that often results in a diffuse spread of infection throughout the medullary spaces, with subsequent necrosis of bone .”

• Etiology – Dental infection

• Clinical features –1. Severe pain , trismus , paresthesia of lip 2. Elevation of temprature 3. Regional lymphadenopathy 4. Pus may exude through gingival pocket 5. In maxilla , infection spread is local, while in

mandible its diffuse .

Radiographic appearance -

Chronic Suppurative Osteomyelitis

• Chronic suppurative osteomyelitis may develop in inadequately treated acute osteomyelitis or may arise from dental infection without preceding acute stage.

• Etiology – 1. Followed by acute osteomyelitis2. Dental infection

• Clinical features –1. Mild pain , trismus , paresthesia of lip 2. Elevation of temprature 3. Regional lymphadenopathy 4. In acute exacerbation ,the suppuration may

perforate the bone , mucosa and overlying skin to form a fistulous tract.

Cutaneous fistula Intraoral fistula with draining abscess

Radiographic appearance -

Chronic Focal Sclerosing Osteomyelitis

• It is an unusual reaction to the mild bacterial infection entering the bone through a carious tooth in persons who have a high degree of tissue resistance and reactivity .

• Here , tissue reacts to the infection by proliferation of cells rather than destruction.

• Etiology – Mild dental infection

• Clinical features –1. No signs and symptoms except for mild pain

due to infected pulp.

• Radiograph –

Chronic Diffuse Sclerosing Osteomyelitis

• It is analogous to the focal form of disease , representing proliferative reaction of the bone diffusely to the low- grade infection.

• Etiology – 1. Generalized periodontal disease.2. Multiple teeth infection (mild)

• Clinical features –

1. No clinical indications of its presence.2. Occasionally , there is acute exacerbation of

the chronic infection results in vague pain , unpleasant taste , mild suppuration &

formation of fistula over the mucosal surface.

• Radiograph-

Garre’s Osteomyelitis

• It is also called as chronic ,non-suppurative osteomyelitis with proliferative periostitis .

• This is distinctive osteomyelitis in which there is focal gross thickening of the periosteum with peripheral reactive bone formation resulting from mild irritation or infection.

• Etiology – Dental infection

• Clinical features-1. Toothache or pain in the jaw 2. Bony hard swelling on the outer surface of

the jaw.

• Radiographic appearance-

Pericoronitis

• Definition –• “Pericoronitis is an inflammation of the gingiva

that covers the chewing surface of the molars which have not fully erupted in the oral cavity. Most commonly , it occurs with third molar which is impacted or erupting .”

Clinical features –

1. Pain 2. Swelling and erythema over the gingiva

covering the tooth .3. Trismus 4. Halitosis 5. Bad taste6. Submandibular lymphadenopathy.

Sialadenitis• It is an inflammatory disease of the major

salivary glands characterized by swelling of the glands believed to be the result of infection.

• Etiology –1. Bacterial or viral infection 2. Mostly occurs in debilitated patients suffering

from dehydration , suppression of salivary secretion or sialolithiasis or after a surgery

Clinical features –

• Oral or facial pain, especially while eating• Erythema over the side of the face or upper neck

(Parotitis)• Swelling (particularly in preauricular region, below

the jaw, or on the floor of the mouth)• Trismus • Fever• Xerostomia • Bad taste • Pus may drain into the mouth.

Parotitis

Sialadenitis of Submandibular gland

Extraoral

Maxillary Sinusitis • Inflammation of mucosa of Maxillary sinus is

Maxillary sinusitis . • Etiology –1. Infection2. Trauma 3. Allergy 4. Infected odontogenic cyst 5. Oroantral communication or fistula 6. Displaced tooth or root

Signs -

Extraoral- 1. Tenderness over cheek . Intraoral- 1. Percussion of maxillary molars show tenderness. 2. Existence of oroantral fistula with or without polypoid mass extruding from socket . 3. Fetor oris on blowing the nose.

Symptoms

1. Nasal blocking following rhinitis 2. Postnasal discharge with constant irritation

requiring clearing of throat.3. Heavy feeling of head.4. Constant throbbing pain in upper part of

cheek or entire side of face which is exacerbated by bending down.

5. Chills , fever ,difficulty in breathing .

Stomatitis • Stomatitis is an inflammation of the mucous lining of any

of the structures in the oral cavity.

Etiology –

• Poor oral hygiene• Dietary protein deficiency• Infections • Iron deficiency anemia • Ill fitting dentures • Mouth burns from hot food or drinks • Medications• Allergic reactions• Radiation therapy

Clinical features

• Pain• Mouth ulcers• Burning sensation• Paresthesia• Bad taste• Excessive salivation

Denture stomatitis

Clinical features

Oral ulcers

Necrotizing fasciitis• “It is defined as a rapidly progressing infection

located in the deep fascia with secondary necrosis of subcutaneous tissue , usually sparing the muscles and accompanied by

high fever ”

Etiology –• Infection- Streptococcus pyogenes

Predisposing factors –• Diabetes mellitus , malignancy , drug addiction

Clinical features-

• High fever .• Erythmatous cellulitis with ill-defined margins • Severe pain but affected area is anesthetized.• Progression of disease is rapid with change in

skin colour from red blue to green in 36 hours • By 4th to 5th day , it leads to cutanous

gangrene.• Skin bullae may devlope• There is no lymphadenopathy.

Acute Necrotizing Ulcerative Gingivits • It is an endogenous oral infection that is characterized

by necrosis of gingiva.

• Etiology –• Infection – Fusiform bacilli , spirochetes

• Predisposing factors –

1. Local factors-• Poor oral hygiene • Preexisting gingivitis• Smoking • Emotional stress

• Systemic factors –• Nutritional deficiency – Vit.- B2 , C

• Debilitating diseases – I. Leukemia II. Aids III. Syphilis

Clinical features –

1. Onset is sudden with Pain , profuse salivation, & metallic taste.

2. Spontaneous gingival bleeding.3. Loss of sense of taste.4. Fetid odor 5. Typical “ Punched out ” crater like ulceration

mostly on interdental papilla ,gingiva becomes brown in colour.

Conclusion

• It is necessary for the oral surgeons to have knowledge about inflammation to diagnose inflammatory diseases and inflammatory lesions and to treat them in Surgical or conservative approach .

References

Books-• Robbin’s Basic Pathology 8th edition • Shafer‘s Textbook Of Oral Pathology 6th edition• Atlas of Pathology

Articles-• Tufts OpenCourseWare © 2008 Tufts University• BJSM article

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