DH228 Chapter 2 Inflammation and Repair

Chapter 2 Inflammation and Repair

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Learning objectives

1. Define each of the words in the vocabulary list forthis chapter.2. With regard to inflammation:• Describe the differences between acute and chronicinflammation.• List and describe the major local and systemic clinical signs ofinflammation.• Describe how the microscopic events are associated witheach of the major clinical signs of inflammation.

3. List the white blood cells that are involved in the inflammatory response and describe how each functions.4. List and describe the biochemical mediators involved in inflammation. 5. List and describe the four major systemic clinical signs of inflammation. 6. Discuss chronic inflammation, as well as antiinflammatory therapy.

The Body’s Responses to Injury: Inflammation, Immunity, and Repair

Injury

Inflammation

• The result of an alteration in the environment that causes tissue damage or necrosis

• Less severe injury: Hyperplasia, hypertrophy, atrophy

• Allows the body to eliminate injurious agents, contain injuries, and heal defects

Innate Defenses

• Physical barrier
• Intact skin or mucosa
• Mechanical defense
• Respiratory system’s cilia and mucus
• Antibacterial activity
• Enzymes in saliva
• Removal of foreign substances
• Flushing action of tears, saliva, urine, and diarrhea
• Inflammation process
• White blood cells

Inflammation

• Nonspecific response
• Extent and duration of injury → extent and duration of inflammatory response
• Local or systemic
• Acute, chronic, or combination

Inflammation: Classic or Cardinal Clinical Signs

• Systemic signs
• Fever
• Leukocytosis
• Elevated C-reactive protein (CRP)
• Lymphadenopathy

• Localized signs
• Redness
• Heat
• Swelling
• Pain
• Loss of normal tissue function

Inflammation: Sequence of Microscopic Events

• Injury to tissue
• Constriction of microcirculation
• Dilation of microcirculation → hyperemia → erythema and heat
• Increase in permeability
• Exudate leaves microcirculation → transudate
• Increased blood viscosity
• Decreased blood flow
• Margination and pavementing of white blood cells (WBCs) → chemotaxis
• WBCs enter tissue → emigration → exudate and edema WBCs ingest foreign material → phagocytosis

Inflammation: Sequence of Microscopic Events

• Transudate
• Exudate
• Edema
• Heat
• Abscess
• Fistula
• Pain

• Hyperemia
• Increased blood flow in capillary beds of injured tissue

• Will produce erythema (redness) and heat
• Exudate
• Increased blood plasma and proteins in injured tissue
• Helps dilute injurious agents but results in excess fluid in tissues: Edema

• Serous (watery) exudate
• Mainly plasma fluids and proteins, a few WBCs
• Purulent exudate (suppuration)
• Contains plasma fluids and proteins, tissue debris, and many WBCs

Inflammation: Vocabulary Review

• Emigration
• The process by which WBCs escape from blood vessels through gaps in endothelial cells

• Chemotaxis
• Directed movement of WBCs toward the site of injury
• Phagocytosis
• The process by which WBCs ingest and then digest foreign substances

• May include pathogenic organisms and tissue debris

White Blood Cells in the Inflammatory Response

White blood cells or leukocytes

• Neutrophils: Polymorphonuclear leukocytes
• Monocytes circulating in blood → macrophages in
• tissue
• Lymphocytes and plasma cells
• Seen in chronic inflammation and the immune response
• Eosinophils and mast cells
• Seen in both inflammation and the immune response

Neutrophils: Polymorphonuclear Leukocytes

• Function
• Phagocytosis
• Microscopic appearance
• Multilobed nucleus and granular cytoplasm that contains lysosomal enzymes

• Constitute 60% to 70% of WBC population
• Derived from stem cells in bone marrow

Macrophages

• Function
• Phagocytosis; play a role in immune system

• Microscopic appearance
• Single round nucleus and do not have granular cytoplasm

• Constitute 3% to 8% of WBC population
• Derived from stem cells in bone marrow

Biochemical Mediators Involved in Inflammation

• Cause many of the events in the inflammatory response

• Basic mediators can recruit other mediators and immune mechanisms
• May be derived from:
• Blood
• Endothelial cells
• White blood cells and platelets
• Pathogenic organisms as they injure the tissue

• Three interrelated systems
• Interaction takes place during activation, among their products, and within their various actions

• Kinin system
• Clotting mechanism
• Complement system

Kinin System

• Active in early phases of inflammation
• Activated by substances in plasma and injured
• tissue
• Causes increased:
• Dilation of blood vessels at the site of injury
• Permeability of local blood vessels
• Induces pain

Clotting Mechanism

• Clots blood and mediates inflammation
• Some of the clotting mechanism products that are activated during tissue injury cause local vascular dilation and permeability by activating kinin

Complement System

• Involves the production of a sequential cascade of plasma proteins
• They are present in blood in an inactive form
• A trigger (usually an antibody-antigen complex) initiates the sequence of steps

• These plasma proteins function in inflammation and immunity
• Some components cause WBCs known as mast cells to release histamine

• Histamine causes an increase in vascular permeability and vasodilation

• Other components cause cell death, form chemotactic factors for WBCs, and enhance phagocytosis

Other Biochemical Mediators of Inflammation

• Released by the body
• Prostaglandins
• Cause increased vascular dilation and permeability, tissue pain and redness, and changes in connective tissue (CT)
• Lysosomal enzymes
• Act as chemotactic factors
• May cause damage to connective tissue and to the clot

• Released by pathogenic microorganisms
• Endotoxin
• Produced by cell walls of gram-negative bacteria
• Serves as chemotactic factor; can activate complement, function as an antigen, and damage bone and tissue
• Lysosomal enzymes
• Have a similar chemical composition and action as those released by WBCs

Systemic Clinical Signs of Inflammation

• Fever
• Leukocytosis
• Elevated C-reactive protein
• Lymphadenopathy

Systemic Manifestations of Inflammation: Fever

• Controlled by the hypothalamus
• Pyrogens
• Fever-producing substances produced by WBCs and pathogens
• Pyrogens act on the hypothalamus
• The hypothalamus increases body temperature by way of prostaglandins

Systemic Manifestations of Inflammation: Leukocytosis

• Normal number of WBCs per mm3 of blood: 4000 to 10,000
• In a systemic inflammatory response, the number increases to 10,000 to 30,000/mm3 of blood. This is leukocytosis, or an increase in circulating WBCs
• It is the body’s attempt to provide more cells for phagocytosis
• The type of WBC that is increasing in number can aid in differential diagnosis
• Viral infection: Increase in lymphocytes
• Bacterial infection: Increase in neutrophils
• Allergic reaction: Increase in eosinophils

Systemic Manifestations of Inflammation: Lymphadenopathy

• Enlarged and palpable superficial lymph nodes
• The enlarged nodes occur because of changes in lymphocytes, which are the primary cells of the immune response

• Hyperplasia: An increase in the number of cells
• Hypertrophy: Enlargement of individual cells

Systemic Manifestations of Inflammation: Elevated Levels of C-Reactive Protein

• Produced in the liver
• Interacts with the complement system and the clotting mechanism

• Levels can be used to help assess rheumatoid arthritis and systemic lupus erythematosus

• Used to monitor tissue healing
• Used as early infection detection system
• Chronically increased level is associated with an increased risk for cardiovascular disease

• Possible marker for periodontal disease

Chronic Inflammation

• Caused by persistent injuries
• Repair cannot be completed until source of injury is removed

• Cells involved include:
• Macrophages
• Lymphocytes
• Plasma cells
• Neutrophils
• Monocytes
• Fibroblasts

Chronic Inflammation: Granulomatous Inflammation

• Formation of granuloma: Microscopic groupings of macrophages surrounded by lymphocytes and plasma cells
• These macrophages group together to form multinucleated giant cells
• Associated with foreign body reactions and some infections such as tuberculosis

Antiinflammatory Therapy

• Nonsteroidal antiinflammatory drugs (NSAIDs)
• Acetylsalicylic acid (aspirin)
• Ibuprofen
• Steroidal antiinflammatory drugs
• Prednisone
• Antihistamines

• Cancer treatment drugs
• Methotrexate
• Sulfasalazine
• Leflunomide
• Cyclophosphamid
• Mycophenolate

Reactive Tissue Responses: Hyperplasia, Hypertrophy, and Atrophy

• Hyperplasia
• An increase in the number of cells, often in response to chronic irritation or abrasion

• May return to normal if the insult subsides, or may persist after removal of the irritant

• Hypertrophy
• An increase in the size of cells
• May be seen in cardiac muscle as a response to hypertension

• Atrophy
• A decrease in size or function of a cell, tissue, organ, or entire body

Regeneration and Repair

• Regeneration
• The process by which injured tissue is replaced with tissue identical to that present before the injury
• Repair
• The restoration of damaged or diseased tissues

Microscopic Events: Day of Injury

• Blood flows into injured tissue to produce a clot
• The clot contains fibrin, clumped red blood cells (RBCs), and platelets

Microscopic Events: Day After Injury

• Neutrophils emigrate from the microcirculation into injured tissue in an acute inflammatory response

• Phagocytosis occurs

Microscopic Events: Two Days After Injury

• Monocytes change to macrophages in tissue
• Macrophages continue phagocytosis and secrete growth factors that stimulate growth of new blood vessels in a process called angiogenesis

• Neutrophils are reduced in number
• Fibroblasts increase in number and produce new collagen fibers in a process called fibroplasia

• Granulation tissue (CT) is formed
• Epithelialization, the process by which new surface tissue is created, occurs

• Blood clot acts as a scaffold for new connective tissue
• Lymphocytes and plasma cells migrate to the area as chronic inflammation and the immune response begins

Microscopic Events: Seven Days After Injury

• Inflammatory and immune responses are
• completed, if the source of injury is removed
• Fibrin is digested by tissue enzymes
• It sloughs off and the initial repair is complete
• The new tissue is relatively red
• New epithelium is thin
• New connective tissue is highly vascularized
• Immature collagen fibers are present and fragile
• Fibroblasts differentiate into myofibroblasts

Microscopic Events: Two Weeks After Injury

• Initial granulation tissue and its fibers have been remodeled

• Matured, fibrous connective tissue is called scar tissue

• It is whiter and paler because of increased collagen and decreased vascularity

Microsopic Events During repair Video

https://www.youtube.com/watch?v=7qgyBZFaIds

Factors Affecting Amount of Scar Tissue

• Type of repair
• Healing by primary intention
• Healing by secondary intention
• Healing by tertiary intention

• Heredity
• Strength and flexibility needed in the tissue
• Tissue type

Types of Repair

Healing by primary intention

Healing by tertiary intention

Healing by secondary intention

• The edges of the injury cannot be joined during healing
• A large clot forms, resulting in increased granulation tissue
• May result in excess scar tissue: A keloid

• Delaying surgical tissue repair until infection is resolved
• An injured area may become infected, especially with puncture wounds
• In some situations, an infected injury is left open until infection is controlled

• Healing of an injury in which there is little loss of tissue
• The margins are close together and very little granulation tissue forms

B= Builds (new bone)

Bone Tissue Repair

Osteoblasts create new bone tissue

• Factors delaying bone formation
• Blood supply at site
• Growth factors
• Edema
• Injury
• Infection
• Removal of osteoblast-producing tissues
• Excessive or inadequate movement of bone tissue

• Factors influencing repair of bone
• Nutrition
• Age
• Tobacco use

Factors That Impair Healing

• Systemic factors
• Malnutrition
• Immunosuppression (Chemotherapy)
• Genetic connective tissue disorders
• Metabolic disorders

• Local factors that impair healing
• Bacterial infection (Streptococcus or Staphylococcus)
• Tissue destruction and necrosis
• Hematoma
• Excessive movement of injured tissue
• Poor blood supply

Injuries to Teeth

• Attrition
• Bruxism
• Abrasion
• Abfraction
• Erosion
• Bulimia
• Methamphetamine abuse

Attrition

• Tooth-to-tooth wear
• May be observed in both primary and permanent dentition

Attrition

TTT = Tooth To Tooth

Bruxism

• Grinding and clenching teeth for nonfunctional purposes such as:

• Occlusal interferences
• Stress
• Tension
• Seizure disorders

Attrition of teeth resulting from bruxism

X = a cross; when grinding we are crossing our teeth back and forth

Bruxism Cont.

• Management
• Occlusal adjustments to eliminate occlusal interferences and fabrication of an acrylic splint

• Signs and symptoms
• Wear facets
• Abnormal rate of attrition
• Hypertrophy of masticatory muscles
• Increased muscle tone
• Muscle tenderness
• Muscle fatigue
• Cheek biting
• Pain in the temporomandibular (TM) joint area
• Tooth mobility
• Pulpal sensitivity to cold

Attrition of teeth resulting from bruxism

X = a cross; when grinding we are crossing our teeth back and forth

Abrasion

• Pathologic wearing away of tooth structure that results from a repetitive mechanical habit

• Most frequently seen as a notching on root surfaces with gingival recession

Abrasion

BR = Buccal surface @ the Root surface BR = most commonly due to improper toothBRushing

Abfraction

• Cause: Microfracture of tooth structure in areas of concentration of stress

• May be related to fatigue, flexure, fracture, and deformation of tooth structure

• May occur in combination with abrasion
• Appearance: Typically appears as wedge-shaped lesions at the cervical areas of teeth

• Preventive treatment: Fabricating an acrylic splint

Abfraction

Fract = microfracture in tooth

Erosion

• Loss of tooth structure as a result of chemicals, without bacterial involvement

• Tooth structure may be lost around a restoration, making the restoration stand out, distinguishing it from abrasion or attrition

• Correlate location of erosion and abrasion with patient’s history

Erosion

Erosion Cont.

• Potential causes
• Industrial factors
• Intraorally applied cocaine hydrochloride drug abuse
• Overuse of soft drinks
• Baby bottle caries
• Sucking on lemons
• Chronic vomiting

Erosion

Bulimia

• An eating disorder characterized by food binges followed by self-induced vomiting

• The patient with bulimia maintains a normal body weight but is secretive about eating habits

• May see electrolyte imbalance and/or malnutrition
• Irritation of oral mucosa and lips
• Traumatic lesions on the backs of the fingers

• Management of oral health
• Fluoride rinse and toothpaste
• Rinse with water after purging
• Avoid brushing immediately after vomiting
• Use very soft toothbrush
• May require full-coverage restorative dental treatment

Methamphetamine Abuse: “Meth Mouth”

• Rapid destruction of teeth as a result of:
• Methamphetamine acid content
• Decreased salivary flow
• Cravings for high-sugar beverages
• Lack of oral hygiene

Meth Mouth

Injuries to Oral Soft Tissue

• Melanosis
• Solar cheilitis
• Mucocele
• Necrotizing sialometaplasia
• Sialolith
• Acute and chronic sialadenitis

• Traumatic ulcer
• Frictional keratosis
• Linea alba
• Nicotinic stomatitis
• Tobacco pouch keratosis
• Traumatic neuroma
• Amalgam tattoo

• Aspirin burn
• Phenol burns
• Electric burns
• Other burns
• Lesions associated with cocaine use
• Lesions from self-induced injuries
• Hematoma

Aspirin Burn

• Topical application is a common misuse of this product

• The tissue becomes necrotic and white
• The surface may slough off, leaving a painful ulcer
• The ulcer usually heals in 7 to 21 days

Phenol Burn

• Used in dentistry as a cavity-sterilizing agent and a cauterizing agent

• Will cause whitening and sloughing of the area as a result of tissue destruction

Dental Materials That Can Cause Burns

• Phenol
• Sodium hypochlorite
• Ferric sulfate
• Formocresol
• Eugenol

• May be seen in infants or young children who have chewed an electrical cord

• May be quite extensive, damaging oral tissue and even tooth buds

• May cause permanent disfigurement and scarring
• Treatment
• Plastic surgery
• Oral surgery
• Orthodontic therapy

Electric Burn

Thermal Burns

• Hot food burns
• From soup or cheese on pizza
• Products containing hydrogen peroxide or eugenol

Lesions Associated With Cocaine Use

• Lesions located at the midline of the hard palate may vary from ulcers to keratotic lesions to exophytic reactive lesions as a result of smoking crack cocaine

• Necrotic ulcers of the tongue and epiglottis have been reported as a result of freebasing cocaine

Ulcer at midline due to crack cocaine

Perforation of midline due to cocaine use

Lesions From Self-Induced Injuries

• Chronic lip, cheek, or tongue biting
• Trauma to the gingiva from a fingernail
• Lesions may range from ulceration to epithelial hyperplasia and hyperkeratosis

Trauma to gingiva from finger nail

Traumatic Ulcer

• Cheek, lip, or tongue biting
• Denture irritation
• Mucosal injury
• Overzealous brushing
• Treatment
• Usually heals within 7 to 14 days unless the trauma persists

• May require a biopsy

Traumatic Ulcer

Traumatic Granuloma

• The result of persistent trauma
• Appearance: Hard (indurated), raised lesion
• Heals rapidly after biopsy

Traumatic Granuloma

Hematoma

• Accumulation of blood within tissue as a result of trauma

• Appears as a red to purple to bluish-gray mass
• Frequently seen on labial or buccal mucosa

Hematoma

Frictional Keratosis

• Treatment
• Identify the traumatic cause of the lesion
• Eliminate the cause
• Must be differentiated from idiopathic leukoplakia because leukoplakia may be premalignant

• A form of hyperkeratosis
• Cause: Chronic rubbing or friction against an oral mucosal surface; resembles a callus on skin
• Appearance: Opaque white

Linea Alba

• A white, raised line most commonly on the buccal mucosa at the occlusal plane

• May be the result of a teeth-clenching habit
• Sometimes the pattern of the teeth can be seen in the lesion

• Microscopic appearance: Epithelial hyperplasia and hyperkeratosis

• No treatment necessary

Nicotine Stomatitis

• A benign lesion typically associated with pipe and/or cigar smoking; may also occur with cigarette smoking

• Initial appearance: Erythema
• Increased opacity as keratinization occurs
• Raised red areas occur at the openings of ducts of inflamed minor salivary glands

Smokeless Tobacco Keratosis

• A white lesion located where chewing tobacco is placed, most often in the mucobuccal fold

• Early lesions may have a granular or wrinkled appearance

• Long-standing lesions may be more opaquely white and have a corrugated surface

Early Lesion

Long-standing Lesion

Tobacco Pouch Keratosis

• Same as smokeless tobacco keratosis, just another name for it.
• Treatment
• Tobacco cessation
• May require biopsy
• Long-term exposure to chewing tobacco has been associated with increased risk of squamous cell carcinoma

Early Lesion

Long-standing Lesion

Electronic (E-) Cigarettes

• Can be damaging to oral tissues as regular cigarette smoking

• Produce an aerosol or vapor to bring nicotine to the lungs

• Vapor contains toxic chemicals and heavy metals

Traumatic Neuroma

• A lesion caused by injury to a peripheral nerve
• When the nerve sheath of Schwann cells is disrupted, occasionally the proximal end of the damaged nerve proliferates into a mass of nerve and Schwann cells mixed with dense fibrous scar tissue

• Painful, ranging from pain on palpation to severe, intractable pain

• Diagnosis
• Biopsy and microscopic examination
• Treatment
• Surgical excision

Palisaded Encapsulated Neuroma (PEN)

• Benign lesion
• Clinical appearance: Mucosal nodule
• Microscopic appearance: Well-circumscribed lesion that is composed of nerve tissue partially surrounded by fibrous connective tissue

• Considered a reactive, hyperplastic lesion

Amalgam Tattoo

• A flat, bluish-gray lesion of the oral mucosa, caused by the introduction of amalgam into tissue

• May occur during placement or removal of an amalgam restoration or during an extraction

• May be seen in any location in the oral cavity, most commonly on the gingiva or alveolar ridge

• Amalgam particles may be seen on radiograph, aiding in diagnosis
• Patient history may help
• Must be differentiated from malignant melanoma
• Treatment
• None, providing melanoma has been ruled out

Melanosis

• Normal physiologic pigmentation of oral mucosa

• May be genetic
• May occur as a result of inflammation:
• Postinflammatory melanosis
• If presenting as a macule, a biopsy may be warranted

• Labial melanotic macule on vermilion of lips
• Smoker’s melanosis

Solar Cheilitis (Actinic Cheilitis)

• A degeneration of the tissue of the lips, caused by exposure to the sun

• Appearance
• Lips appear dry and cracked
• The vermilion appears pale pink and mottled
• The interface between lips and skin is indistinct
• Microscopically: Epithelium is thinner than normal; degenerative CT changes

• Smoking and alcohol use increase risk of squamous cell carcinoma
• Biopsy may be indicated for persistent scaling or ulceration
• Prevention
• Avoid sun exposure
• Use sun-blocking agents

Mucous Retention Lesion: Mucocele

• A lesion formed when a salivary gland duct is severed and the mucous salivary gland secretion spills into the adjacent connective tissue

• Not a true cyst because it is not lined with epithelium

Mucous Retention Lesions: Mucocele, Mucous Cyst, or Mucous Retention Cyst

• Dilated salivary gland ducts that developed as a result of duct obstruction

• Treatment
• Removal of affected minor salivary gland

Mucous Retention Lesion: Ranula

• A unilateral mucocele-like lesion that forms on the floor of the mouth

• Associated with the ducts of submandibular and sublingual glands

Sialolith (SIGH-uh-luh-lith)

• A salivary gland stone
• May be found in both minor and major salivary glands

• Formed by precipitation of calcium salts around a central core

• May often be seen on radiographs
• Treatment
• Sometimes the calcification can be “milked” from the duct
• Stimulate salivary flow by sucking on sour lemon candies (sugar free of course) can help

• It may require surgical removal; this may damage the duct

Necrotizing Sialometaplasia

• A benign condition of salivary glands
• Moderately painful swelling and ulceration
• Thought to result from blockage of blood supply to affected area, resulting in salivary gland necrosis

• Salivary gland epithelium is replaced by squamous epithelium

• The ulcer usually heals by secondary intention
• Biopsy is needed to establish diagnosis

Reactive Connective Tissue Hyperplasia

• Pyogenic granuloma
• Giant cell granuloma
• Irritation fibroma
• Denture-induced fibrous hyperplasia
• Papillary hyperplasia of the palate
• Gingival enlargement
• Chronic hyperplastic pulpitis
• Proliferating, exuberant granulation tissue and dense fibrous connective tissue resulting from overzealous repair

• May be a response to a single event or chronic low- grade injury

Pyogenic Granuloma

• Appearance
• Ulcerated
• Soft to palpation
• Bleeds easily
• Deep red to purple
• Generally elevated, may be sessile or pedunculated
• Most commonly observed on the gingiva, it may be seen on other intraoral areas
• May vary in size from a few millimeters to several centimeters
• Usually develops rapidly and then remains static
• Most common in teenagers and young adults, but may occur at any age
• If seen in a pregnant female, it is called a pregnancy tumor
• Treatment
• Surgically excised if it does not regress spontaneously

• A proliferation of connective tissue containing numerous blood vessels and inflammatory cells occurring as a response to injury

• The name is a misnomer; the lesion is neither pyogenic (pus forming) nor a true granuloma

Pregnancy Tumor

• A pyogenic granuloma seen in a pregnant woman

• The lesions are identical to those seen in men and nonpregnant women

• May be caused by hormonal changes and increased response to plaque

• They often regress after delivery

Localized Juvenile Spongiotic Gingivitis (LJSG)

• Recently defined lesion that clinically resembles a pyogenic granuloma

• Thought to arise from improper exteriorization of junctional epithelium

• Seen most commonly in younger patients, with a slight female predilection reported

Peripheral Giant Cell Granuloma

• A lesion that contains many multinucleated giant cells, well-vascularized connective tissue, RBCs, and chronic inflammatory cells

• Reactive lesion
• Clinical appearance resembles that of pyogenic granuloma

• Treatment: Surgical excision

Peripheral Ossifying Fibroma

• Exophytic, usually well-demarcated sessile or pedunculated gingival lesion

• Clinically it appears to emanate from the interdental papilla

• Has been reported in both children and adults
• Composed of cellular fibrous connective tissue
• Treatment consists of complete surgical excision with thorough scaling of the adjacent teeth

Fibroma, Irritation Fibroma, Traumatic Fibroma, and Focal Fibrous Hyperplasia

• The most common mass on the gingiva
• Caused by trauma
• Appearance: A broad-based, persistent exophytic lesion composed of dense, scarlike connective tissue with few blood vessels. Usually a small lesion, less than 1 cm in diameter

Epulis Fissuratum (Denture- Induced Fibrous Hyperplasia)

• Cause: Ill-fitting denture
• Location: In elongated folds of tissue adjacent to denture flange

• Composed of dense, fibrous CT surfaced with stratified squamous epithelium

• Treatment
• Surgical removal
• Relining of prosthesis
• New denture

Inflammatory Papillary Hyperplasia of the Palate

• Denture-induced hyperplasia
• Appearance: Palatal mucosa covered by multiple erythematous papillary projections; “cobblestone” appearance

• Treatment
• Surgical removal of hyperplastic papillary tissue before new denture construction

Gingival Enlargement

• An increase in the bulk of free and attached gingiva, especially the interdental papillae

• Gingival margins are rounded
• Color may vary from normal pink to pale or erythematous depending on the degree of inflammation and vascularity

• May be generalized or localized

Gingival Enlargement Cont.

• Reactive response to:
• Local irritants
• Hormonal changes
• Drugs
• Hereditary conditions
• Idiopathic factors
• Leukemia
• Treatment
• Gingivoplasty
• Gingivectomy
• Meticulous oral hygiene

Chronic Hyperplastic Pulpitis (Pulp Polyp)

• An excessive proliferation of chronically inflamed dental pulp tissue

• Occurs in teeth with large, open carious lesions often in primary and permanent molars

• Usually asymptomatic
• Granulation tissue with inflammatory cells, primarily lymphocytes and plasma cells

• Neutrophils may be present
• Generally surfaced by stratified squamous epithelium

• Treatment
• Endodontic therapy
• Extraction

Inflammatory Periapical Lesions

• Periapical abscess
• Dental or periapical granuloma
• Radicular cyst (periapical cyst)
• Resorption of teeth
• Focal sclerosing osteomyelitis
• Alveolar osteitis (“dry socket”)

Inflammatory Periapical Lesions

• Caries or trauma may result in:
• Inflammation
• Infection
• Chronic hyperplastic pulpitis
• Necrosis of the pulp
• The inflammatory process begins in pulp and then extends to the periapical area
• Accessory canals may lead to areas of inflammation on the lateral portion of the root

Periapical Abscess

• Acute periapical abscess: Purulent exudate surrounded by connective tissue containing neutrophils and lymphocytes

• Inflammation produces severe pain
• Tooth may slightly extrude from tooth socket
• May or may not test positive with electric pulp testing

Apical = located at apex (PA radiograph Abscess = Acute

Periapical Abscess Cont.

• Fistula
• Fistulous tract
• Channel of least resistance
• Presence of fistula warrants a radiographic evaluation

Periapical Abscess Cont.

• May develop directly from inflammation in the pulp

• More commonly develops in an area of previously existing chronic inflammation

• Treatment
• Drainage and endodontic therapy
• Extraction

Periapical Granuloma

• A localized mass of chronically inflamed granulation tissue that forms at the opening of the pulp canal, generally at the apex of a nonvital tooth root
• Characteristics
• Chronic process
• Most cases are asymptomatic
• Tooth may be sensitive to pressure and percussion
• Tooth may be slightly extruded from the socket
• Treatment
• Endodontic therapy
• Extraction

Periapical = apex Granuloma = Granulation tissue

Periapical Granuloma Cont.

• Composed of granulation tissue containing lymphocytes, plasma cells, and macrophages

• May also contain neutrophils, areas of dense fibrous connective tissue, or epithelial rests of Malassez

Periapical Abscess vs. granuloma

• Periapical Abscess:
• Acute
• Pus-filled infection
• Intense pain and swelling

• Periapical Granuloma:
• Chronic
• Granulation of tissue
• Asymptomatic or mild symptoms

VS.

Radicular Cyst (Periapical Cyst)

• Radiographic appearance
• Radiolucent
• Well circumscribed
• Same as periapical granuloma
• Treatment
• Endodontic therapy
• Apicoectomy
• Extraction and curettage of periapical tissue

• A true epithelium-lined cyst
• Associated with the root of a nonvital tooth
• The most commonly occurring cyst in the oral region
• A result of proliferation of the rests of Malassez
• Usually asymptomatic and discovered on radiograph

Residual Cyst

• Forms after tooth extraction and all or part of radicular cyst is left behind

• Treatment
• Surgical removal

Tooth Resorption

• External resorption: Nonreversible resorption of the tooth structure, beginning at the outside of the tooth

• Causes
• Inflammation
• Pressure
• Reimplantation
• Idiopathic

External Root Resorption

Tooth Resorption

• Internal tooth or root resorption: Resorption often associated with an inflammatory response in the pulp or an idiopathic reason

• Appearance
• Clinically: A pinkish area in the crown resulting from the vascular, inflamed connective tissue

• Radiographically: Radiolucent

Internal tooth resorption

Tooth Resorption

• Treatment of internal or root resorption
• If the root is not perforated, calcium hydroxide is placed and endodontic treatment is performed in an attempt to save the tooth

• If the tooth is perforated, it must be removed

Tooth Resorption External vs Internal

• Internal:
• Begins inside the tooth/root
• Radiolucent
• Internal = Inside

• External:
• Begins outside the tooth/root
• External =outside

Focal Sclerosing Osteomyelitis (Condensing Osteitis)

• A change in the bone near the apices of teeth
• Thought to be a reaction to low-grade infection
• Generally asymptomatic
• If painful, may be associated with pulpal inflammatory disease

Focal Sclerosing Osteomyelitis (Condensing Osteitis)

• Radiopaque
• Borders may be diffuse or well defined
• Commonly associated with the mandibular first molar

• No treatment usually necessary
• Biopsy to rule out other radiopaque lesions such as osteoma, complex odontoma, or ossifying fibroma

Alveolar Osteitis (“Dry Socket”)

• A postoperative complication following tooth removal in which the blood clot is lost before healing can take place, leaving raw, exposed nerve endings

• Most often occurring in mandibular third molar areas
• Patient may complain of pain, bad odor, and bad taste
• Risk factors
• Dissolution of the clot at the surgical site
• Traumatic extraction
• Presence of infection before extraction
• Tobacco smoking after extraction

Alveolar Osteitis (“Dry Socket”)

• Treatment
• Gentle irrigation
• Daily application of Dry Socket Paste containing eucalyptol until symptoms are relieved

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