inflammation and repair Flashcards

1
Q

Adaptive Reactive Tissue Responses

A

Atrophy: decreasing in size
Hypertrophy: increasing cell size
Hyperplasia: increased cell number
Metaplasia: conversion of one cell type to another
Dysplasia: disorderly growth

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2
Q

What is inflammation?

A

non-specific response to injury involving microcirculation and its blood vessels.

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3
Q

What are the key steps in the inflammatory process?

A
  1. Offending agent is recognized by the host.
  2. Leukocytes and plasma proteins are recruited to the site.
  3. Leukocytes and proteins act to destroy and remove the offending agent.
  4. The reaction is regulated and terminated.
  5. Damaged tissue is repaired.
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4
Q

What causes inflammation?

A

Microbes (bacteria, virus, fungus)
Physical injury (trauma, thermal, etc)
Allergens/ hypersensitivity
Chemical irritants (drugs, toxins, etc)
Inflammatory disorders
Foreign bodies (splinters, sutures, etc)

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5
Q

inflammation of the pulp

A

Pulpitis

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6
Q

inflammation of salivary glands

A

Sialadenitis

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7
Q

inflammation of the tongue

A

Glossitis

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8
Q

inflammation of the papilla

A

Papillitis

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9
Q

inflammation of the mucosa

A

Mucositis

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10
Q

inflammation of the oral mucosa

A

Stomatitis

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11
Q

inflammation of the lips

A

Cheilitis

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12
Q

inflammation of the bone

A

Osteitis

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13
Q

inflammation of the bone and marrow spaces

A

Osteomyelitis

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14
Q

What are the two types of white blood cells initially involved in the inflammatory response?

A

Neutrophils and monocytes.

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15
Q

What is the primary function of neutrophils in inflammation?

A

Phagocytosis; they are the first white blood cells recruited and die shortly after.

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16
Q

What distinguishes neutrophils structurally?

A

They have a multilobed nucleus, also known as polymorphonuclear leukocytes.

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17
Q

What role do monocytes/macrophages play in inflammation?

A

They perform phagocytosis and play an important role in the immune response.

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18
Q

What is the difference between monocytes and macrophages?

A

Monocytes are in the bloodstream, and they are called macrophages when they migrate into tissues.

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19
Q

How does the host recognize an offending agent in inflammation?

A

Epithelial cells, macrophages, dendritic cells, leukocytes, and other cells express receptors to sense microbes and damage, while circulating proteins recognize microbes in the blood.

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20
Q

What are pattern recognition receptors (PRRs) and their function?

A

receptors on innate immune cells that recognize pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) linked to cell stress.

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21
Q

How are leukocytes and plasma proteins recruited to the site of injury or infection?

A

Changes in blood flow and vessel permeability (vasodilation) maximize movement of plasma proteins and leukocytes to the site.

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22
Q

What is the process of leukocyte movement during recruitment to injury sites?

A

Displace to the periphery of the blood vessel
Loosely attach and roll on the endothelium
Adhere to the endothelium
Migrate through interendothelial spaces
Move to the injury site via chemotaxis, guided by biochemical mediators.

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23
Q

What is edema?

A

excess accumulation of plasma or exudate in the interstitial space, causing tissue swelling.

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24
Q

What is serous exudate?

A

clear fluid that may flow out of tissue when further injured.

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25
Q

What is purulent exudate or suppuration?

A

thick yellow-white pus containing white blood cells.

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26
Q

What is an abscess?

A

collection of purulent exudate.

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27
Q

What is phagocytosis?

A

ingestion and digestion of particulate material by cells.

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28
Q

What are the steps of phagocytosis?

A

Recognition and attachment of the particle to be ingested.
Engulfment with the formation of a phagocytic vacuole.
Killing or degradation of the ingested material by free radicals.

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29
Q

How is the acute inflammatory reaction terminated?

A

Anti-inflammatory mediators regulate and terminate the reaction when it is no longer needed.

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30
Q

Major Localized Clinical Signs

A

Dolor/ pain
Calor/ heat
Rubor/ redness
Tumor/ swelling
Loss of function

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31
Q

Major Systemic Clinical Signs

A

Fever
Leukocytosis
Lymphadenopathy
Elevated C-reactive protein

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32
Q

What defines fever as a systemic clinical sign?

A

Body temperature higher than 98.6ºF caused by fever-inducing substances (pyrogens) from white blood cells and pathogenic microorganisms.

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33
Q

What is leukocytosis?

A

An increase in white blood cells circulating in the blood to provide more cells for phagocytosis, occurring in response to infection, pregnancy, cancer, or hematologic disorders.

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34
Q

How is leukocytosis assessed?

A

By performing a complete blood count (CBC).

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35
Q

What is elevated C-reactive protein (CRP)?

A

A non-specific protein produced in the liver in response to inflammation.

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36
Q

What is lymphadenopathy?

A

Enlargement of lymph nodes due to hyperplasia and hypertrophy; lymphoid tissue in Waldeyer’s ring can also enlarge.

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37
Q

What are the three possible outcomes of acute inflammatory reactions?

A

Complete resolution: Tissue regeneration replaces injured tissue with identical tissue.
Healing by connective tissue replacement: Tissue repair restores damaged tissue through cellular change and growth (scarring or fibrosis).
Progression to chronic inflammation.

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38
Q

What is tissue regeneration?

A

The process by which injured tissue is replaced with identical tissue present before the injury.

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39
Q

What is tissue repair?

A

The restoration of damaged or diseased tissue through cellular change and growth, often resulting in scarring or fibrosis.

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40
Q

What happens on the day of injury during tissue healing?

A

Immediate formation of a blood clot with fibrin, red blood cells, and platelets.

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41
Q

What occurs one day after injury?

A

Acute inflammation begins, and neutrophils migrate from microcirculation into the injured tissue.

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42
Q

What happens two days after injury?

A

Monocytes migrate from microcirculation into the injured tissue, fibroblasts proliferate, and new blood vessels form (angiogenesis).

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43
Q

What happens seven days after injury?

A

Inflammation and immune response are completed if the injury source is removed. Myofibroblasts contract.

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44
Q

What occurs two weeks after injury?

A

Granulation tissue is removed, and mature fibrous connective tissue (scar) persists.

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45
Q

What is the initial tissue formed during the healing process?

A

Granulation tissue.

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46
Q

What is formed during the healing process as the new surface layer?

A

Epithelization forms the new surface layer.

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47
Q

What is hemostasis?

A

orchestrated process involving platelets, clotting factors, and endothelium that occurs at the site of vascular injury, resulting in the formation of a blood clot to prevent or limit bleeding.

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48
Q

What is granulation tissue?

A

tissue is composed of fibroblasts, new blood vessels, and leukocytes. It has a pink, soft, granular appearance and forms as part of the healing process, with the amount depending on the size of the injury and the intensity of inflammation.

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49
Q

What are the types of repair?

A

Primary intention
Example: surgical incision
Secondary intention
Example: healing of tooth extraction
Tertiary intention
Example: complication due to infection

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50
Q

What are local factors that impair healing?

A

Bacterial infection, necrotic tissue, hematoma (hemorrhage), poor blood supply, and history of irradiation to the area.

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51
Q

What are systemic factors that impair healing?

A

Diabetes, malnutrition, immunodeficiency, immunosuppression, tobacco use, and age.

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52
Q

What is the onset and duration of acute inflammation?

A

rapid onset
developing within minutes, and lasts from a few hours to days.

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53
Q

What happens to the tissue during acute inflammation?

A

Tissue returns to its original state or repair begins immediately.

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54
Q

What causes chronic inflammation to persist?

A

caused by persistent causative agents, such as difficult-to-eradicate microorganisms, hypersensitivity diseases, or prolonged exposure to toxins.

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55
Q

How long does chronic inflammation last?

A

weeks, months, or even indefinitely.

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56
Q

What are the outcomes of chronic inflammation?

A

leads to more extensive tissue destruction, slower healing, and is associated with more serious functional deficiencies.

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57
Q

Which inflammatory cells are involved in chronic inflammation?

A

Macrophages, lymphocytes, and plasma cells

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58
Q

What is a distinct form of chronic inflammation?

A

Granulomatous inflammation

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59
Q

What is attrition?

A

wearing away of tooth structure due to tooth-to-tooth contact.

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60
Q

What is abrasion?

A

wearing away of tooth structure from repetitive mechanical habits.

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61
Q

What is abfraction?

A

wedge-shaped defect at the cervical area of teeth, typically due to stress and flexing of the tooth.

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62
Q

What is erosion?

A

loss of tooth structure caused by chemical action, often from acidic substances.

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63
Q

What are the signs and symptoms of bruxism?

A

Grinding of teeth for non-functional purposes
Wear facets on the occlusal surface of teeth
Enlargement and tenderness of masticatory muscles
TMJ pain
Tooth mobility or sensitivity
Attrition

64
Q

What are the effects of aggressive toothbrush use on teeth?

A

Improper brushing technique (back-and-forth scrubbing motion)
Use of abrasive toothpaste or hard toothbrush
Horizontal wear on the cervical aspect of the tooth root in areas of gingival recession
Abrasion

65
Q

How does bulimia affect oral health?

A

It can lead to loss of tooth structure on the lingual aspect of teeth due to exposure to stomach acid from vomiting.
Erosion

66
Q

What type of traumatic tooth injury is associated with methamphetamine use?

A

an cause severe tooth decay, erosion, and “meth mouth,” characterized by widespread dental damage, including loss of tooth structure and decay due to acidic content, decreased saliva flow, and poor oral hygiene.

67
Q

What happens when a patient places aspirin tablet directly on painful tooth?

A

Tissue becomes necrotic
Painful and heals slowly due to extent of destruction

68
Q

What endodontic material can cause mucosal necrosis?

A

Rubber dam, formocresol or sodium hypochlorite

69
Q

What causes oral mucosal burns from hot food?

A

Thermal burns from food or liquids that are too hot, commonly occurring on the palate or tongue, common from microwaved food

70
Q

How can cotton rolls cause oral mucosal burns?

A

drying and ripping the tissue when removed, or by absorbing caustic materials (such as chemicals or medications) in the area, which may cause irritation or injury to the mucosa.

71
Q

How can mouthwash cause oral mucosal burns?

A

Mouthwash and toothpaste containing alcohol can cause sloughing of the epithelium (skin cells) with overuse, leading to irritation or burns of the oral mucosa.

72
Q

How do electrical burns affect the oral mucosa?

A

typically occur when infants or young adults chew on live electrical cords, causing burns to the oral mucosa. These burns can result in tissue damage and, in severe cases, permanent disfigurement

73
Q

What oral lesion is associated with chronic cocaine use?

A

Palatal perforations, which can occur with chronic cocaine

74
Q

How long does a traumatic ulcer take to heal if trauma is removed?

75
Q

How long can a traumatic ulcer last if trauma persists?

A

weeks or even months

76
Q

Why is a biopsy recommended for a traumatic ulcer?

A

rule out oral cancer and to ensure the lesion is not malignant

77
Q

What is Traumatic Ulcerative Granuloma with Stromal Eosinophilia (TUGSE)?

A

rare, non-cancerous condition that can cause prolonged ulceration with an eosinophilic infiltrate in the tissue, often related to trauma

78
Q

What is a hematoma?

A

lesion caused by the accumulation of blood within tissue as a result of trauma, leading to a localized swelling or bruise.

79
Q

What is frictional keratosis?

A

condition caused by chronic rubbing or friction, leading to hyperkeratosis (thickening of the skin) in the affected area.

80
Q

How is frictional keratosis diagnosed?

A

identifying the trauma causing the condition, eliminating the source of friction, and observing the resolution of the lesion.

81
Q

What does nicotine stomatitis look like?

A

white “cracked mud” appearance and red dots, which are inflamed minor salivary glands.

82
Q

What is nicotine stomatitis?

A

condition characterized by changes to the palate due to long-term pipe and cigar use, likely caused by the heat. its reversible

83
Q

Why is it important to distinguish frictional keratosis from other white lesions?

A

It must be differentiated from other white lesions to rule out conditions such as leukoplakia or other potentially malignant disorders.

84
Q

What is smokeless tobacco keratosis?

A

tissue alterations occur at the site where smokeless tobacco is placed, often presenting as a white, wrinkled appearance. its reversible

85
Q

What microscopic changes might be observed in smokeless tobacco keratosis?

A

may show epithelial dysplasia under microscopic examination, classifying it as an oral potentially malignant disorder.

86
Q

What is a traumatic neuroma?

A

reactive lesion caused by injury to a peripheral nerve, resulting in a proliferation of nerve tissue into a nodule.

87
Q

What happens to the damaged nerve in a traumatic neuroma?

A

proliferates into a mass of small nerve bundles surrounded by connective tissue

88
Q

How does a traumatic neuroma present clinically?

A

painful nodule

89
Q

How is a traumatic neuroma diagnosed?

90
Q

T or F: Amalgam Tattoo is a Iatrogenic lesion

91
Q

melanin pigmentation occurring after an inflammatory response is?

A

Post-inflammatory melanosis

92
Q

melanin pigmentation occurring in association with smoking is?

A

Smoker’s melanosis

93
Q

What microscopic changes might be seen in actinic cheilitis?

A

It may contain epithelial dysplasia, making it an oral potentially malignant disorder.

94
Q

What is an oral (labial) melanotic macule?

A

flat, well-circumscribed lesion characterized by focal deposition of melanin in the oral or labial tissues. Its cause is unknown, and it appears as a flat, brown-to-black spot

95
Q

What is a mucocele?

A

lesion caused by damage to a salivary gland duct, leading to pooling of saliva in the connective tissue and triggering an inflammatory response that walls off the mucous.

96
Q

Where is the most common location for a mucocele?

97
Q

How does a mucocele present clinically?

A

swelling that often fluctuates in size over time

98
Q

What is a ranula?

A

mucocele that occurs on the floor of the mouth

99
Q

What is a Sialolith?

A

Salivary Gland Stone

100
Q

What is a pyogenic granuloma?

A

common benign, reactive lesion characterized by the proliferation of connective tissue with numerous blood vessels and inflammation.

101
Q

How does a pyogenic granuloma present clinically?

A

painless, red, exophytic mass, often with an ulcer, that bleeds easily.

102
Q

What is the most common location for a pyogenic granuloma?

103
Q

Why is the term “pyogenic granuloma” a misnomer?

A

does not produce purulent exudate (pyogenic) and is not a true granuloma histologically

104
Q

In which population are pyogenic granulomas common?

A

pregnant women

105
Q

What is a peripheral giant cell granuloma (PGCG)?

A

reactive lesion composed of vascular connective tissue and multinucleated giant cells.

106
Q

How does PGCG present clinically?

A

appears as a painless, red, exophytic mass, often with an ulcer that bleeds easily.

107
Q

Where is PGCG located?

A

The lesion is peripheral, occurring outside the bone on the gingiva. (Central giant cell granuloma occurs inside the bone.)

108
Q

What lesion can PGCG resemble?

A

pyogenic granuloma

109
Q

What is a peripheral ossifying fibroma (POF)?

A

An exophytic mass occurring on the gingiva that contains scattered bone and cementum-like calcifications.

110
Q

Where does POF clinically appear to originate?

A

interdental papilla

111
Q

What is the origin of POF?

A

periodontal ligament

112
Q

What is the treatment for POF?

A

Complete surgical removal along with scaling of adjacent teeth to prevent recurrence.

113
Q

What lesions can POF clinically resemble?

A

It can appear similar to a pyogenic granuloma or peripheral giant cell granuloma.

114
Q

What are the 3Ps in the differential diagnosis of gingival lesions?

A

Pyogenic granuloma, peripheral giant cell granuloma (PGCG), and peripheral ossifying fibroma (POF).

115
Q

What is the treatment for the 3Ps?

A

Surgical excision of the lesion and submission for microscopic examination to confirm the diagnosis.

116
Q

What is spongiotic gingival hyperplasia?

A

recently defined lesion, most commonly seen on the maxillary facial gingiva of young patients, with a female predilection.

117
Q

How does spongiotic gingival hyperplasia respond to oral hygiene?

A

It does not improve with oral hygiene.

118
Q

How does spongiotic gingival hyperplasia present clinically?

A

localized, flat to slightly papillary, red patch on the gingiva.

119
Q

What treatment has shown some success for spongiotic gingival hyperplasia?

A

Topical steroid application

120
Q

What is a fibroma?

A

A very common exophytic lesion composed of dense connective tissue, typically resulting from trauma.

121
Q

What is epulis fissuratum?

A

A lesion caused by an ill-fitting denture, typically located in the vestibule along the denture flange.

122
Q

How is a fibroma treated?

A

It is removed surgically and submitted for microscopic examination to confirm the diagnosis.

123
Q

What is inflammatory papillary hyperplasia?

A

A condition associated with ill-fitting maxillary complete or partial dentures, characterized by erythematous and granular tissue.

124
Q

How is epulis fissuratum treated?

A

The lesion is removed surgically, examined microscopically, and the denture is either relined or a new one is constructed to prevent recurrence.

125
Q

What is a common infection seen with inflammatory papillary hyperplasia?

A

It is usually superficially infected with Candida albicans, contributing to the erythematous appearance.

126
Q

How is inflammatory papillary hyperplasia treated?

A

addressing the ill-fitting denture, possibly antifungal therapy for the Candida infection, and ensuring proper denture fit.

127
Q

What causes gingival hyperplasia in the context of chronic inflammation?

A

Local irritants such as biofilm and calculus contribute to chronic inflammation, which can lead to gingival hyperplasia (an abnormal increase in gum tissue).

128
Q

How do hormonal changes contribute to gingival hyperplasia?

A

Hormonal changes during pregnancy and puberty

129
Q

What medications can cause gingival hyperplasia?

A

Medications that can lead to gingival hyperplasia include:

Calcium channel blockers (commonly prescribed for hypertension).
Anti-seizure medications (such as phenytoin).
Cyclosporine (an immunosuppressant used in organ transplants).

130
Q

What is a pulp polyp?

A

A pulp polyp is the excessive proliferation of chronically inflamed dental pulp tissue, typically in response to an ongoing pulp infection or injury. May need rct or ext

131
Q

How does a pulp polyp present clinically?

A

It is usually asymptomatic, with the tissue often protruding from the tooth and appearing red or pink.

132
Q

What is a periapical abscess?

A

acute and painful condition characterized by the accumulation of purulent exudate (pus) at the apex of a non-vital tooth, caused by bacterial infection.

133
Q

What types of cells are involved in a periapical abscess?

A

contains neutrophils and lymphocytes, which are involved in the immune response to the infection.

134
Q

What is a parulis?

A

mass of granulation tissue that forms at the mucosal opening of a fistulous tract, often seen with a periapical abscess. It is commonly referred to as a “gum boil.”

135
Q

What is a rare but serious complication of a periapical abscess?

A

Ludwig angina is a rare but serious complication that can cause airway obstruction and requires immediate medical attention.

136
Q

What is a periapical granuloma?

A

localized mass of chronically inflamed granulation tissue at the apex of a non-vital tooth, often seen as a radiolucency on dental X-rays. May need rct or ext

137
Q

How does a periapical granuloma present clinically?

A

asymptomatic, but the affected tooth is usually sensitive to percussion.

138
Q

What types of cells are involved in a periapical granuloma?

A

Lymphocytes, plasma cells, and macrophages are the key cells present in a periapical granuloma.

139
Q

What is a radicular cyst?

A

abnormal, epithelial-lined cavity surrounded by a fibrous connective tissue wall, typically located at the apex of a non-vital tooth. May need rct or ext

140
Q

How does a radicular cyst appear on a radiograph?

A

radiolucency at the apex of a non-vital tooth, similar to a periapical granuloma.

141
Q

What is a residual cyst?

A

forms when a tooth is removed but the cyst is left behind, potentially leading to continued cystic growth.

142
Q

Can a radicular cyst be differentiated from a periapical granuloma on a radiograph alone?

A

No, it is not reliably possible to differentiate a periapical granuloma from a radicular cyst based on radiographs alone.

143
Q

What is tooth resorption?

A

process where tooth structure is broken down and absorbed by the body. It can occur as part of normal exfoliation of deciduous (baby) teeth.

144
Q

What are the two types of tooth resorption?

A

external or internal. External resorption occurs on the outer surface of the tooth, while internal resorption happens within the pulp chamber or root canal.

145
Q

What causes tooth resorption?

A

inflammation is present, such as in cases of infection or trauma.

146
Q

Can tooth resorption be associated with orthodontic therapy?

A

Yes, external root resorption can occur as a result of orthodontic therapy, typically due to the forces applied to the tooth during treatment.

147
Q

What is idiopathic osteosclerosis?

A

form of osteosclerosis that is not associated with inflammation or infection. It occurs without any clear cause.

148
Q

What is osteosclerosis?

A

increased density of bone, appearing radiopaque on X-rays.

149
Q

What is condensing osteitis?

A

change in the bone near the apices of teeth, typically a response to low-grade infection, such as chronic pulpitis. It appears as a radiopaque area on radiographs.

150
Q

How does condensing osteitis differ from idiopathic osteosclerosis?

A

associated with a low-grade infection or inflammation, while idiopathic osteosclerosis is not related to any infection or inflammation.

151
Q

What is alveolar osteitis?

A

also known as “dry socket,” is a postoperative complication following tooth extraction where the blood clot is lost prematurely before healing can occur.

152
Q

When do symptoms of alveolar osteitis typically appear?

A

pain, swelling, bad odor, and bad taste usually appear 1-3 days after the extraction.

153
Q

Which area is most frequently affected by alveolar osteitis?

A

The mandibular third molar extraction site

154
Q

What factors increase the risk of developing alveolar osteitis?

A

Tobacco smoking, using a straw directly after extraction, and spitting heavily are risk factors for developing dry socket.

155
Q

Loss of tooth structure caused by chemical action describes?

156
Q

A ranula is located on the?

A

Floor of the mouth

157
Q

Which of the following is the body’s initial response to injury?

A

Inflammatory response