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dentistry year 4: module 7 > Oral Pathology > Flashcards

Oral Pathology Flashcards

1-52 - OP 1/2: Intro to Oral Cancers/White Lesions 53-61 - OP 3: Red Lesions 62-84 - OP4: Pigmented Lesions 85-118 - OP5: Ulcerated Lesions 119-157 - OP6: Oral Cancer 158-172 - OP7: Non-Cystic Dental inflam lesions 173-209 - OP8: Odontogenic Cysts 210-217 - OP9: Non Odontogenic Cysts 218-252 - OP10: Odontogenic Tumors 253-296 - OP11: Bone Pathology

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1
Q

What is Leukoplakia?

A

Leukoplakia is a white patch that develops in the mouth. The condition is usually painless but is closely linked to an increased risk of mouth cancer

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2
Q

What is Proliferative Verrucous Leukoplakia?

A

Proliferative verrucous Leukoplakia (PVL) is a rare type of oral Leukoplakia, where white patches that have a high risk of becoming cancerous develop inside the mouth. It mainly involves the lining inside of the cheeks (buccal mucosa) and tongue.

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3
Q

What are Fordyce spots?

A

Are ectopic sebaceous glands which tend to be seen on the lip and buccal mucosa, becoming more prominent as patient get older. This is an example of developmental white lesion. Fordyce spots are harmless and painless.

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4
Q

What is Leukoedema?

A

Leukoedema is a white or whitish-grey oedematous lesion of the buccal and labial oral mucosa. The lesions may be diffuse or patchy and are usually asymptomatic. Leukoedema may be confused with Leucoplakia.

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5
Q

What is white sponge naevus?

A

White sponge nevus is a hereditary autosomal dominant condition characterized by the formation of white patches of tissue called nevi (singular: nevus) that appear as thickened, velvety, sponge-like tissue. The nevi are most found on the moist lining of the mouth (oral mucosa), especially on the inside of the cheeks

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6
Q

What is pachyonychia congenita?

A

Pachyonychia congenita is a rare genetic disorder characterized mainly by hypertrophy of the nails and hyperkeratosis of the skin and mucosae.

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7
Q

What is Dyskeratosis congenita?

A

Dyskeratosis congenita (DC) is an inherited bone marrow failure syndrome that is characterized by lacey reticular hyperpigmentation of the skin, dystrophic nails, mucous membrane Leucoplakia and pancytopenia. Diagnosis may be delayed until clinical signs are apparent.

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8
Q

What is Oral lichen planus?

A

(LIE-kun PLAY-nus) is an ongoing (chronic) inflammatory condition that affects mucous membranes inside your mouth. Oral lichen planus may appear as white, lacy patches; red, swollen tissues; or open sores. These lesions may cause burning, pain or other discomfort.

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9
Q

What is the pathogenesis for lichen planus?

A

T cell-mediated immunological damage to the basal cells of epithelium.

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10
Q

What are basal cells?

A

Basal cells are found at the bottom of the epidermis — the outermost layer of skin. Basal cells produce new skin cells. As new skin cells are produced, they push older cells toward the skin’s surface, where the old cells die and are sloughed off

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11
Q

Oral lesions are typically found in what percentage of patients who suffer from skin lesions?

A

50%

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12
Q

If skin lesions are described as violaceous, what does that mean?

A

They are of a violet colour.

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13
Q

Which surface is the common site for lichen planus to develop?

A

Flexor surface of the wrist is the most common site, here skin lesions develop slowly and 85% resolve within 18 months.

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14
Q

In contrast oral LP runs a more chronic course, sometimes several years. Oral lesions are usually bilateral or unilateral?

A

Bilateral and often symmetrical.

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15
Q

Where is the mist common location for oral lichen planus?

A

Buccal mucosa

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16
Q

A spectrum of appearances may be observed, alone or in various combinations for oral lichen planus, what best describes reticular appearance?

A

characterized by a fine network or netlike structure

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17
Q

A spectrum of appearances may be observed, alone or in various combinations for oral lichen planus, what best describes atrophic appearance?

A

Diffuse red lesions resembling erythroplakia.

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18
Q

A spectrum of appearances may be observed, alone or in various combinations for oral lichen planus, what best describes papular appearance?

A

Small white papules that may coalesce (come together to form one mass)

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19
Q

A spectrum of appearances may be observed, alone or in various combinations for oral lichen planus, what best describes erosive appearance?

A

Extensive areas of shallow ulceration

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20
Q

A spectrum of appearances may be observed, alone or in various combinations for oral lichen planus, what best describes bullous appearance?

A

Development of subepithelial bullae (blisters)

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21
Q

This dense, band-like infiltrate (dark purple) of lymphocytes hugging epithelial/connective tissue junction is shown histopathological to which oral condition?

A

Lichen planus

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22
Q

The histopathological slide of lichen planus shows that the epithelial layer has undergone what?

A

Hyperkeratosis.

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23
Q

Histopathology of lichenoid inflammation- not exclusive to lichen planus!

Therefore, close correlation with clinical findings is very important

Features of lichenoid inflammation is also seen in.

A
  1. Lichenoid reaction to drugs/restorative materials
  2. Lupus erythematosus
  3. Graft-versus-host disease
  4. Lichenoid inflammation associated with dysplasia
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24
Q

Why is Lichen Planus an oral potentially malignant disorder (OMPD)?

A

Because they have the potential risk of developing into oral squamous cell carcinoma.

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25
Q

Treatment for symptomatic Lichen Planus includes steroids, how do steroids affect the body?

A

Steroids also reduce the activity of the immune system, which is the body’s natural defence against illness and infection. This can help treat autoimmune conditions, such as rheumatoid arthritis or lupus, which are caused by the immune system mistakenly attacking the body.

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26
Q

Which medication can cause oral lichen planus?

A

Systemic medications such as beta blockers, nonsteroidal anti-inflammatory drugs, anti-malarial, diuretics, oral hypoglycaemics, penicillamine, oral retroviral medications are reported to initiate or exacerbate oral lichen planus and oral lichenoid reaction.

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27
Q

What is lupus erythematosus?

A

Lupus is an autoimmune disorder which attacks healthy part of your body, including soft tissues.

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28
Q

Candidosis, syphilitic leukoplakia, oral hairy leukoplakia all causes oral white lesions, however they fall under which class of white lesions?

A

Infective.

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29
Q

What is candidiasis?

A

Candidiasis is a fungal infection caused by a yeast (a type of fungus) called Candida.

Some species of Candida can cause infection in people; the most common is Candida albicans.

Candida normally lives on skin and inside the body, such as the mouth, throat, gut, and vagina, without causing problems.

Candida can cause infections if it grows out of control or if it enters deep into the body. For example, it can cause infections in the bloodstream or internal organs like the kidney, heart, or brain.

Oral thrush is a fungal infection of the mouth. It is not contagious and is usually successfully treated with antifungal medication.

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30
Q

What is syphilitic leukoplakia?

A

This term refers to a white lesion associated with syphilis, specifically in the tertiary stage of the infection. It is not considered to be a type of idiopathic leukoplakia, since the causative agent Treponema pallidum is known

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31
Q

What is oral hairy leukoplakia?

A

Oral hairy leukoplakia is a condition triggered by the Epstein-Barr virus (EBV). It causes white patches on your tongue. Sometimes the patches happen in other parts of your mouth. The patches may look hairy. This is where the name comes from.

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32
Q

What is meant by idiopathic?

A

relating to or denoting any disease or condition which arises spontaneously or for which the cause is unknown.

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33
Q

What causes Leukoplakia, proliferative verrucous leukoplakia?

A

The cause is yet unknown, these conditions are known as idiopathic.

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34
Q

What is meant by neoplastic?

A

A neoplasm is an abnormal growth of cells, also known as a tumour. Neoplastic diseases are conditions that cause tumour growth.

Growth can be either benign (noncancerous) or malignant (cancerous). Benign tumours usually grow slowly and can’t spread to other tissues.

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35
Q

What is meant by dysplastic lesions?

A

A term used to describe the presence of abnormal cells within a tissue or organ. Dysplasia is not cancer, but it may sometimes become cancer. Dysplasia can be mild, moderate, or severe, depending on how abnormal the cells look under a microscope and how much of the tissue or organ is affected.

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36
Q

What are squamous cells?

A

Squamous cells: These are flat cells in the upper (outer) part of the epidermis, which are constantly shed as new one’s form.

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37
Q

What is squamous cell carcinoma?

A

Squamous cell carcinoma (SCC) of the skin is the second most common form of skin cancer, characterized by abnormal, accelerated growth of squamous cells.

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38
Q

What is meant by ill defined margins?

A

Ill definition of the margins of a lesion is a common, though nonspecific, characteristic that suggests a malignant process. Ill-defined margins are often due to superimposed normal breast tissues obscuring the margins of a lesion.

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39
Q

White sponge naevus usually appears bilaterally or unilaterally?

A

Bilaterally, can present anywhere in the oral mucosa but is typically seen in the buccal mucosa.

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40
Q

What other areas of the body can white sponge naevus affect?

A

Nose, oesophagus and anogenital region.

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41
Q

What is hyperparakeratosis?

A

Hyperkeratosis refers to thickening of your skin’s outer layer

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42
Q

What is acanthosis?

A

Acanthosis nigricans (AN) is a mucocutaneous disorder of unclear origin characterized by the presence of hyperpigmented papillary lesions on the skin and papillomatous lesions in the oral cavity.

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43
Q

What is histopathology?

A

Histopathology refers to the microscopic examination of tissue in order to study the manifestations of disease

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44
Q

What is atypia?

A

State of being not typical or normal, in medicine, atypia is an abnormality in cells in tissue.

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45
Q

What are parakeratinized cells?

A

parakeratinized epithelium + An epithelium that is characterized by incomplete keratinization of the cells in the stratum corneum. The cells are flattened and composed primarily of packed tonofilaments. However, the cells may retain remnants of nuclei and other organelles.

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46
Q

What is a prickle cell?

A

Also known as a spinous cell is an epidermal cell that, as a histological artifact, develops numerous intercellular bridges that give it a prickly appearance.

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47
Q

What is the lamina propria?

A

A type of connective tissue found under the thin layer of tissues covering a mucous membrane

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48
Q

What are the treatment options for white sponge naevus?

A

None required

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49
Q

This basket appearance marked by the blue circle is indicative in which hereditary oral condition?

A

White sponge naevus.

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50
Q

Roughened white patch at site of chronic trauma is indicative of frictional keratosis, what would you expect to see histopathological?

A

Hyperkeratosis and prominent scarring fibrosis within submucosa

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51
Q

What is squamous cell carcinoma?

A

Squamous cell carcinoma (SCC) of the skin is the second most common form of skin cancer, characterized by abnormal, accelerated growth of squamous cells.

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52
Q

How do you treat frictional keratosis?

A

Should resolve when source of friction removed

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53
Q

What is median rhomboid glossitis?

A

Median rhomboid glossitis (MRG) is defined as the central papillary atrophy of the tongue.

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54
Q

What is erythroplakia?

A

Erythroplakia means “red patch” and refers to a lesion with a reddish appearance that doesn’t have another obvious cause. They appear in the mouth or throat. They tend to be flat and have a velvety texture. They may have white spots on them. Some have a tendency to bleed easily.

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55
Q

There is no treatment for geographic tongue however patients are told to avoid which type of food?

A

Spicy/acidic

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56
Q

Can dysplastic lesions, squamous cell carcinoma present as a red patch?

A

Yes

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57
Q

Median rhomboid glossitis aetiology is uncertain, however in most cases it is associated with which type of infection candida.
Histopathological view would show the loss of what on the dorsum of the tongue?

A

Lingual papillae

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58
Q

What would you expect to see histopathologicaly of median rhomboid glossitis?

A
  1. Loss of lingual papillae
  2. Parakeratosis and acanthosis of the squamous epithelium
  3. Candidal hyphae in parakeratin and associated neutrophils
  4. Chronic inflammatory infiltrate in connective tissue
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59
Q

Treatments for median rhomboid glossitis includes antifungal medication, regardless of the success of the treatment, what part of the tongue cannot be fixed?

A

The lingual papillae on the dorsum of the tongue will not grow back.

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60
Q

Erythroplakia and speckled leukoplakias have high likelihood of malignant transformation of what percentage?

A

(50%)

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61
Q

What form of leukoplakia is this?

A

Speckled leukoplakia

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62
Q

What is meant by exogenous?

A

having an external cause or origin.

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63
Q

What is meant by endogenous?

A

having an internal cause or origin.

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64
Q

Oral pigmentation can arise from exogenous causing superficial staining of mucosa such as?

A
  1. Foods
  2. Drinks
  3. Tobacco
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65
Q

What is hyperplasia?

A

An increase in the number of cells in an organ or tissue. These cells appear normal under a microscope. They are not cancer, but may become cancer

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66
Q

What is black hairy tongue?

A

Black hairy tongue is caused by an overgrowth of dead skin cells, causing lengthening of the papillae, and staining from bacteria, yeast, food, tobacco or other substances in the mouth. Black hairy tongue is a temporary, harmless oral condition that gives the tongue a dark, furry appearance.

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67
Q

What is the aetiology of an amalgam tattoo?

A

Amalgam introduced into socket/mucosa during treatment, presents as asymptomatic blue/black lesion, which can be seen in radiographs.

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68
Q

Amalgam tattoo can be associated which layers of the soft tissues?

A

Associated with collagen, elastic fibres and basement membranes.

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69
Q

If an amalgam tattoo cannot be seen on a radiograph what is the process for a diagnosis?

A

May be excised to confirm diagnosis.

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70
Q

What is melanotic macule?

A

Oral melanotic macule is a non-cancerous (benign), dark spot found on the lips or inside the mouth. An oral melanotic macule found on the lip is sometimes called a labial melanotic macule.

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71
Q

What causes a melanotic macule?

A

Melanotic macules usually arise from three sources: an intraoral freckle, postinflammatory pigmentation, or disorders such as Addison’s disease, Peutz-Jeghers syndrome, or Laugier-Hunziker syndrome. Although the melanotic macule does not develop due to sun exposure, its origin is not conclusive.

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72
Q

What are pigmented nevi?

A

Pigmented nevi (moles) are growths on the skin that usually are flesh-coloured, brown or black. Moles can appear anywhere on the skin, alone or in groups. Moles occur when cells in the skin grow in a cluster instead of being spread throughout the skin

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73
Q

What is Peutz-Jeghers syndromes?

A

Peutz-Jeghers syndromes (PJS) is a genetic disorder. People with PJS develop polyps and dark-coloured spots that appear on various parts of the body and are at greater risk for some types of cancer. Include multiple pigmented lesions on skin/mucosa, lips, tongue, palate, buccal mucosa, intestinal polyposis.

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74
Q

What is smoker’s melanosis?

A

Smoker’s melanosis (see Right) is increased tissue pigmentation, or darkening, due to irritation from tobacco smoke. Typically, this pigmentation occurs on the gingiva (gums) of the upper and lower front teeth

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75
Q

What is melanotic neuroectodermal tumour of infancy?

A

Melanotic neuroectodermal tumour of infancy (MNTI) is a rapidly growing benign tumour arising from the neural crest cells. It typically affects infants and occurs in the head and neck region.

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76
Q

What is mucosal melanoma?

A

Mucosal melanoma (MM) is a rare melanoma subtype that originates from melanocytes within sun-protected mucous membranes. Compared with cutaneous melanoma (CM), MM has worse prognosis and lacks effective treatment options

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77
Q

Melanotic macules are benign legions caused by increased activity of melanocytes, these are most found where?

A

Buccal mucosa, palate and gingiva most common sites. They are frequently excised to confirm diagnosis and exclude melanoma.

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78
Q

Histologically what would you expect to see for a melanotic macule?

A
  1. Increased melanin pigment in basal keratinocytes – not increased number of melanocytes
  2. Melanin pigmentary incontinence in underlying connective tissue
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79
Q

Mucosal melanoma is a malignant neoplasm of what?

A

Melanocytes

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80
Q

What are melanocytes?

A

A cell in the skin and eyes that produces and contains the pigment called melanin.

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81
Q

How does mucosal melanoma present at first in terms of symptoms?

A

Presents as asymptomatic. May remain unnoticed until pain, ulceration, bleeding or a neck mass.

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82
Q

What is the prognosis of mucosal melanoma?

A

Prognosis is poor, as it is typically very advanced at presentation, very invasive and metastasise early. Biology of mucosal melanomas is different from skin melanomas.

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83
Q

What doe the term pleomorphic mean?

A

Occurring in various distinct forms. In terms of cells, having variation in the size and shape of cells or their nuclei.

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84
Q

What is the treatment option for mucosal melanoma?

A

Surgical resection is mainstay treatment along with adjuvant radiotherapy.

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85
Q

What is an Ulcer?

A

localized surface defect with loss of epithelium exposing underlying inflamed connective tissue

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86
Q

Ulcers are associated with haematological disease, GI disease, HIV, what are these types of diseases?

A

Systemic disease.

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87
Q

Ulcers are associated with lichen planus, discoid lupus erythematosus, immunobullous disease, what are these types of disease?

A

Dermatological disease

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88
Q

What type of ulcer is this?

A

Aphthous

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89
Q

What type of ulcer is this?

A

Traumatic

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90
Q

Why is it extremely important that cause for traumatic ulcer is identified?

A

If no apparent cause is found with what appears to be a traumatic ulcer, then further investigations is warranted.

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91
Q

What does this image show?

A

Ulcerated squamous cell carcinoma, this can easily be mistaken as traumatic ulcer, hence the urgency to determine the diagnosis.

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92
Q

Why is it difficult to differentiate between the types of ulcers?

A

A large proportion of ulcers will show non-specific features, ulceration with loss of surface epithelium, inflamed fibrinoid exudate and inflamed granulation tissue.

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93
Q

If a vesicle is a small blister, what is a bulla?

A

Bulla is a blister with a diameter greater than 10mm

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94
Q

A subset of lesions are known as immunobullous disorder, what is this?

A

These are autoimmune diseases on which autoantibodies against components of skin and mucosa produce blisters.

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95
Q

Disorders which result in vesicles/bullae can be classified histologically depending on the location of the bulla, which are?

A
  1. Intraepithelial
  2. Subepithelial
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96
Q

Intraepithelial bullae can be further classified in to two groups what are they?

A
  • Non-acantholytic (death and rupture of cells) eg viral infection such as HSZ
  • Acantholytic (desmosomal breakdown)
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97
Q

What does acantholysis mean?

A

Means loss of coherence between epidermal cells due to the breakdown of intracellular bridges.

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98
Q

What are the stages for a intraepithelial non-acantholytic bullae?

A
  1. Virus targets and replicates within epithelial cells
  2. Leads to cell lysis
  3. Groups of infected cells breakdown to form vesicles within the epithelium
  4. Infected cells infect nearby normal cells and an ulcer forms when the full thickness of the epithelium is involved and is destroyed
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99
Q

What is a bullae?

A

A bulla is a fluid sac or lesion that appears when fluid is trapped under a thin layer of your skin.

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100
Q

What is pemphigus?

A

Pemphigus is a disease that causes blistering of the skin and the inside of the mouth, nose, throat, eyes, and genitals.

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101
Q

What is pemphigus vulgaris?

A

Is a rare group of autoimmune diseases. It causes blisters on the skin and mucous membranes throughout the body.

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102
Q

Pemphigus vulgaris is most frequently found in which sex and affects which ages?

A

Most frequently found in females ages 40-60.

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103
Q

What are autoantibodies?

A

An antibody produced by an organism in response to a constituent of its own tissues.

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104
Q

What is the treatment for pemphigus vulgaris?

A

Steroids

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105
Q

Which studies is used in combination of routine histopathology to confirm diagnosis of pemphigus vulgaris?

A

Direct immunofluorescence (DIF) studies.

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106
Q

What type of specimen needs to be provided for Direct Immunofluorescence?

A

Fresh specimen

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107
Q

These are examples of what type of lesions?

  1. Pemphigoid
  2. Erythema multiforme
  3. Dermatitis herpetiformis
  4. Epidermolysis bullosa acquisita
A

Subepithelial

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108
Q

What is pemphigoid?

A

Bullous pemphigoid is a rare skin condition that mainly affects older people. It usually starts with an itchy, raised rash. As the condition develops, large blisters can form on the skin. It may last a few years and sometimes causes serious problems, but treatment can help manage the condition in most cases

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109
Q

What is erythema multiforme?

A

Erythema multiforme is a skin reaction that can be triggered by an infection or some medicines. It’s usually mild and goes away in a few weeks. There’s also a rare, severe form that can affect the mouth, genitals and eyes and can be life-threatening. This is known as erythema multiforme major

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110
Q

What is Dermatitis Herpetiformis?

A

Dermatitis herpetiformis (DH) is a chronic, intensely itchy, blistering skin manifestation of gluten-sensitive enteropathy, commonly known as celiac disease. DH is a rash that affects about 10 percent of people with celiac disease

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111
Q

What is Epidermolysis bullosa acquisita?

A

Epidermolysis bullosa acquisita (EBA) is an acquired form of EB with similar symptoms. Like EB, EBA causes the skin to blister easily. It can also affect the mouth, throat and digestive tract. But EBA isn’t inherited, and symptoms don’t usually appear until later life.

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112
Q

The following belong to a group of?

  1. Bullous Pemphigoid
  2. Mucous Membrane Pemphigoid
  3. Linear IgA disease
  4. Drug-induced Pemphigoid
A

Autoimmune diseases

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113
Q

Which of the pemphigoid diseases is the most common orally?

A

Mucus membrane pemphigoid. Oral mucosa almost always involved and usually first affected site. Gingiva, buccal mucosa, tongue, palate.

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114
Q

With mucous membrane pemphigoid the bullae tend to be relatively tough, why?

A

Bullae tend to be relatively tough as the ‘lid’ is full thickness epithelium. When they rupture tend to heal slowly with scarring. Ocular lesions can lead to blindness.

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115
Q

What is the treatment for mucous membrane pemphigoid?

A

Steroids

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116
Q

What type of specimen is required for DIF for mucous membrane pemphigoid?

A

Fresh specimen

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117
Q

How many variants of epidermolysis bullosa is there?

A

3 variants

  1. Simplex- intraepithelial, mutations in keratins 5/14
  2. Junctional- subepithelial, separation in lamina lucida, laminin mutations
  3. Dystrophic- subepithelial, separation beneath basal lamina, mutation in type VII collagen gene
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118
Q

What is the name of the blood bullosa that presents on the palate?

A

Angina bullosa haemorrhagica

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119
Q

What is the name of this oral cancer?

A

Oral Submucous Fibrosis

120
Q

What is Oral submucous fibrosis?

A

(OSMF) is an oral precancerous condition characterized by inflammation and progressive fibrosis of the submucosal tissues resulting in marked rigidity and trismus.

121
Q

What is a complication with vascularity, in areas present with submucous fibrosis?

A

Decreased vascularity

122
Q

Oral submucous fibrosis (OSF) is characterized by abnormal deposition of what?

A

Collagen

123
Q

It is a precancerous disorder and transforms into a malignant tumour in what percentage of all cases?

A

1.5–15%

124
Q

Symptoms of oral submucous fibrosis include?

A

Symptoms include submucous fibrosis, ulceration, xerostomia, a burning sensation, and restricted mouth opening.

125
Q

Oral submucous fibrosis (OSF) patients experience a severe burning sensation in the mouth after ingesting what type of food?

A

spicy foods.

126
Q

Epidemiological studies have shown that the most significant risk factors for OSF is?

A

Chewing betel nut

127
Q

If you look histologically for oral submucous fibrosis, would you see marked epithelial atrophy or trophic?

A
128
Q

What is chronic hyperplastic candidiasis?

A

Chronic hyperplastic candidiasis (CHC), earlier known as candida leucoplakia, is a variant of oral candidiasis that classically presents as a white patch on the commissures of the oral mucosa, and it is mostly caused by Candida albicans.

129
Q

Chronic candidiasis also known as chronic hyperplastic candidiasis is a persistent white patch on oral mucosa, can it be removed by scraping?

A

No

130
Q

The commissure of the oral mucosa is commonly involved in cases of chronic candidiasis, where else can it be involved?

A

Palate or tongue

131
Q

Which other oral condition is often associated with chronic candidiasis, when it is present on the commissure of the oral mucosa?

A

Angular cheilitis

132
Q

What are the histological features of epithelial dysplasia?

A
  1. Nuclear and cellular pleomorphism
  2. Alteration in nuclear/cytoplasmic ratio (invariably an increase)
  3. Nuclear hyperchromatism
  4. Prominent nucleoli
  5. Increased and abnormal mitoses
  6. Loss of polarity of basal cells
  7. Basal cell hyperplasia
  8. Drop-shaped rete pegs ie wider at their deepest part
  9. Irregular epithelial stratification or disturbed maturation
  10. Abnormal keratinization ‘Dyskeratosis’- cell starts to keratinize before the surface is reached)
  11. Loss/ reduction of intercellular adhesion
133
Q

The degree of dysplasia is classified using a grading of score what?

A

WHO 2017 grading mild, moderate, severe = carcinoma in situ.

134
Q

WHO 2017 Grading- based on 1/3 of epithelium, for epithelial dysplasia (mild, moderate, severe)
* Mild
* Moderate
* Severe

A
  • Mild- disorganisation, increased proliferation and atypia of basal cells
  • Moderate- more layers of disorganised basaloid cells, atypia, suprabasal mitoses
  • Severe- very abnormal, affects full thickness of epithelium
135
Q

What would you grade these histological slides for epithelial dysplasia?

A
136
Q

What are the management of epithelial dysplasia?

A
  1. Modify risk factors
  2. High risk sites
  3. Antifungal treatment
  4. Excision/ Co2 Laser Excision
  5. ? Topical agents
  6. Close Clinical Review
  7. Rebiopsy
137
Q

What is this type of cancer?

A

Squamous cell carcinoma

138
Q

5 year survival remains = poorer than many other cancers?

A

55%

139
Q

What are the screening programs for oral cancer?

A

No screening program.

140
Q

What are the risk factors for oral squamous cell carcinoma?

A
  • Tobacco
  • Alcohol
  • Betel quid/pan/areca nut
  • Previous oral cancer
  • Exposure to UV light (lip)
  • Poor diet
  • Immune suppression
  • Genetics??
  • Social deprivation
  • ?? HPV- Oropharyngeal cancer
141
Q

What are the intraoral sites that are high risk for oral cancer?

A
  • High risk sites-
  • lateral/ventral tongue,
  • floor of mouth,
  • retromolar trigone (tonsils/soft palate-oropharyngeal)
142
Q

What are the early detection additional detection tests for oral cancer not including visual examination?

A
  1. Toludine blue
  2. Autofluorescene
  3. Chemiluminescence
  4. Vizlite plus
  5. Sensitivity/specificity
143
Q

Scottish Referral Guidelines for Suspected Cancer

A

*Urgent ‘suspicion of cancer’ referral
*To Specialist Management Team ie for suspected oral cancer refer to Oral & Maxillofacial Surgery
*Formal written referral with full details
*2 weeks

144
Q

Referral guidelines
* Persistent unexplained head and neck lump > 3 weeks
* Unexplained ulceration or unexplained swelling/induration of the oral mucosa persisting > 3weeks
* All unexplained red or mixed red and white patches of the oral mucosa persisting > 3weeks
* Persistent (not intermittent) hoarseness lasting for > 3weeks
* Persistent pain in the throat or pain on swallowing lasting for > 3weeks

A
145
Q

diagnosis of SCC is confirmed by?

A

Biopsy

146
Q

very poorly differentiated tumours may require what to confirm diagnosis?

A

Immunochemistry

147
Q

what is SCC graded by degree of what?

A

Differentiation:
* Well-differentiated tumour cells very obviously squamous with ‘prickles’ and keratinization

  • Moderately differentiated
  • Poorly differentiated, may be difficult to identify tumour cells as epithelial
148
Q

What are the treatment options for SCC?

A
  • Surgery
  • +/- adjuvant therapy
  • Monoclonal antibodies
    5yr survival not improved over last few decades
149
Q

‘TNM Classification of Malignant Tumours’ used for most cancers including external lip and oral cavity carcinomas, what does TNM stand for?

A

TNM components:

T- extent of primary tumour

N- absence or presence and extent of regional lymph node metastasis

M- category describes the absence or presence of distant metastasis

Each component is given a number, the higher the number the more extensive the disease, poorer prognosis (T1N0M0, T4N2M1)

150
Q

What clinical data is included in the ‘core data items included in the histopathology report’?

A
  1. Site and laterality of tumour (TUMOUR LATERALITY identifies the side of the body for a Tumour relating to paired organs within a PATIENT.)
  2. Type of specimen
151
Q

What pathological data is included in the ‘core data items included in the pathology report’?

A
  1. Maximum diameter of tumour
  2. Maximum depth of invasion
  3. Histological type of carcinoma
  4. Degree of differentiation (grade)
  5. Pattern of invasion
  6. Distance from invasive carcinoma to surgical margins
  7. Vascular invasion
  8. Nerve invasion
  9. Bone invasion
  10. Severe dysplasia/carcinoma-in-situ
152
Q

What pathological data is included in the core pathological data for neck dissection specimens?

A
  1. Total number of lymph nodes at each anatomic level
  2. Number of nodes involved by metastatic carcinoma
  3. Size of the largest metastatic deposit
  4. Extracapsular spread
153
Q

Under the 8th edition of staging what does this staging mean?

A
  • Tx Primary tumour cannot be assessed
  • T0 No evidence of primary tumour
  • Tis Carcinoma in Situ
  • T1 Tumour 20 mm or less in greatest dimension and 5mm or less depth of invasion
  • T2 Tumour 2cm or less in greatest dimension and more than 5mm but no more than 10mm depth of invasion or Tumour more than 2 cm but not more than 4 cm in greatest dimension and depth of invasion no more than 10mm
  • T3 Tumour >4 cm in greatest dimension or more than 10mm depth of invasion
154
Q

Staging of T4a (lip) indicates what:

A

T4a (Lip) Tumour invades through cortical bone, inferior alveolar nerve, floor of mouth or skin (chin or nose

155
Q

Staging of T4a (oral cavity) indicates what:

A

T4a (Oral cavity) Tumour invades through cortical bone of the mandible or maxillary sinus, or invades skin of face

156
Q

Staging of T4b (lip and oral cavity) indicates what:

A

T4b (Lip and Oral cavity) tumour invades masticator space, pterygoid plates, or skull base, and/or encases internal carotid artery

157
Q

pN staging is staging of what?

A

Regional lymph nodes

158
Q

Periradicular/periapical inflammation is most often due to bacterial infection following?

A

Pulpal death. Pulpal death is most commonly due to caries, though may be subsequent to trauma.

159
Q

What is a periapical granuloma?

A

Periapical granuloma is one of the most common of all sequelae of pulpitis. It is essentially a localised mass of chronic granulation tissue formed in response to the infection. The involved tooth is sensitive to percussion, and the patient feels pain while chewing solid food.

160
Q

What are the clinical features of Acute periradicular periodontitis?

A
  1. History of pain
  2. Grossly carious/heavily restored tooth
  3. Previous trauma
  4. Typically, little to see radiographically unless acute exacerbation of chronic lesion
161
Q

Histopathology: what would you expect to see in acute periradicular periodontitis?

A
  1. Vascular dilation
  2. Neutrophils
  3. Oedema
162
Q

What are the treatment options for acute periradicular periodontitis?

A
  1. Extraction or endodontic treatment
163
Q

Acute and chronic periradicular periodontitis can lead to a periapical abscess, what are the clinical features for this?

A
  1. Pain
  2. Swelling/sinus
164
Q

Histologically you would expect to see in acute and chronic periradicular periodontitis a central collection of pus which includes neutrophils, bacteria, cellular debris, adjacent to this collection of pus what would you also expect to see.

A

Adjacent zone of preserved neutrophils.

165
Q

What are the treatment options for acute periapical abscess?

A
  1. Drainage and extraction
  2. Endodontic treatment
166
Q

Chronic periradicular periodontitis may follow acute periodontitis or be chronic from the onset, what are the clinical features:

A
  1. Non-vital tooth, may be previous RCT
  2. Often minimal symptoms
  3. Apical radiolucent may be evident on radiograph
167
Q

Histologically you would expect to see what in chronic periradicular periodontitis?

A
  • Lymphocytes
  • Plasma Cells
  • Macrophages
  • Granulation tissue progressing to fibrosis
  • Resorption of bone
  • Minimal, if any, tooth resorption
168
Q

What are the treatment options for chronic periradicular periodontitis?

A
  1. Extraction
  2. Endodontic treatment
  3. Endodontic retreatment
  4. Periradicular surgery
169
Q

What is a periapical granuloma?

A

Is a mass of inflamed granulation issue at the apex of a non-vital tooth, not a true granuloma, can transform to an abscess and some may undergo cystic change (radicular cyst).

170
Q

What are the typical clinical features of a chronic periradicular periodontitis on radiographs?

A

Radiolucent lesion typically evident on radiograph.

171
Q

What are the treatment options for periapical granuloma?

A
  1. Extraction
  2. Endodontic treatment
  3. Endodontic retreatment
  4. Periradicular surgery
172
Q

What are the treatment options for pericoronitis?

A
  1. Irrigation
  2. Consider extraction of opposing tooth
  3. Antibiotics
173
Q

What is a cyst?

A
  • A pathological cavity having fluid or semi- fluid content
  • Lined wholly or in part by epithelium
  • Not due to accumulation of pus- abscess
174
Q

Cysts of the jaws can be classified as what?

A
  • Odontogenic
  • Non-Odontogenic
175
Q

Odontogenic cysts derive from where?

A

Derived from epithelial residues of tooth-forming organ (inflammatory, developmental)

176
Q

Non-odontogenic cysts derive from where?

A

Derived from sources other than tooth-forming organ

177
Q

Where do teeth develop from?

A

Odontogenic epithelium and neural crest derived ectomesenchyme, the dental lamina buds down from the ectoderm and becomes the enamel organ.

178
Q

What are the 4 layers of the enamel organ during odontogenesis?

A

4 layers of the enamel organ-
1. Inner enamel epithelium (future ameloblasts)
2. Outer enamel epithelium
3. Stellate reticulum
4. Stratum intermedium

179
Q

Remnants of odontogenic epithelium remain in the periodontal ligament and gingiva after tooth development, what are the remnants of the dental lamina and root sheath of hertwig known as?

A
  • Remnants of the dental lamina, known as the Glands of Serres
  • Remnants of the Root Sheath of Hertwig, persist as Cell Rests of Malassez
180
Q

Odontogenic cysts that are a result from inflammatory or developmental factors all derive from what?

A

Derived from epithelial residues of tooth-forming organ

181
Q

Inflammatory odontogenic cysts can be divided in two cysts what are they?

A

Radicular cysts and inflammatory collateral cysts.

182
Q

Radicular cysts can be classified in two three groups what are they?

A
  1. Apical
  2. Lateral
  3. Residual
183
Q

Inflammatory collateral cysts can be broken down to two categories, what are they?

A
  1. Paradental cyst
  2. Mandibular buccal bifurcation cyst
184
Q

What is the most common type of jaw cyst?

A

(55% odontogenic cysts)

185
Q

A radicular cyst is a slow growing swelling and often no symptoms are present unless very large, thus a radicular cyst MUST be associated with a vital/non vital tooth?

A

Non-vital tooth

186
Q

With the radicular cyst being a slow growing swelling, how would describe the radiolucent lesion seen at the apex?

A

Typically, well-circumscribed unilocular radiolucent lesion.

187
Q

What are the treatment options for radicular cyst?

A

Small cysts may resolve after
1. RCT
2. Extraction
3. periradicular surgery.
4. Enucleation—removal of the entire cyst. A mucoperiosteal flap is raised overlying the cyst and the entire cyst subsequently removed.
5. Marsupialisation for very large lesions

188
Q

What is a lateral radicular cyst?

A

Radicular cyst arising from a lateral root canal branch of a non-vital tooth

189
Q

What is a residual cyst?

A

residual cyst that persists after extraction of the associated non-vital tooth

190
Q

What are the 2 variants of inflammatory collateral cysts?

A
  1. Paradental cyst – lower third molars
  2. Mandibular buccal bifurcation cyst – lower 1st or 2nd molars
191
Q

60% of inflammatory collateral cysts are paradental cysts, what are their clinical features?

A

. Long-standing pericoronitis
* Associated with vital tooth
* Well-demarcated radiolucency

192
Q

What are the clinical features of a, mandibular buccal bifurcation cyst?

A
  • Often painless swelling
  • Associated tooth usually tilted buccally with deep perio pocket
  • Well-demarcated buccal radiolucency
193
Q

What is the best possible treatment option for paradental and mandibular buccal infiltration cyst?

A

Enucleation

194
Q

The following arise from what type of cysts?

  1. Odontogenic keratocyst
  2. Dentigerous cyst
  3. Eruption cyst
  4. Lateral periodontal cyst and Botryoid odontogenic cyst
  5. Glandular odontogenic cyst
  6. Gingival cysts
  7. Calcifying odontogenic cyst
  8. Orthokeratinized odontogenic cyst
A

Developmental odontogenic cysts

195
Q

Odontogenic keratocyst is seen where in a radiograph?

A

Angle of the mandible

196
Q

What are the treatment options for odontogenic keratocyst?

A
  • Marsupialization
  • Enucleation
  • Marsupialization + Enucleation
  • Enucleation + Carnoy’s solution (modified Carnoy’s)
  • Enucleation + Cryotherapy
  • Resection
197
Q

What are the clinical features of dentigerous cyst?

A
  1. 2nd most common odontogenic cyst
  2. Encloses all or part of crown of unerupted tooth
  3. Attached to Amelocemental junction
  4. Impacted teeth or late to erupt; 3, 5, 8 s
  5. Mandible > Maxilla, 20-50yrs
  6. Symptom-free until significant swelling or if infected
  7. Ballooning expansion
  8. Well-circumscribed unilocular radiolucency associated with crown of unerupted tooth
198
Q

What is the treatment of dentigerous cyst?

A
  1. Enucleation
  2. Exposure/transplantation/extraction of associated tooth
199
Q

What is an eruption cyst and what are the clinical features?

A

Eruption cyst = dentigerous cyst arising in extra-alveolar location, clinical features are:
* Typically seen in children
* Deciduous and permanent molars
* Presents as bluish swelling

200
Q

What is an eruption cyst and what are the clinical features?

A

Eruption cyst = dentigerous cyst arising in extra-alveolar location, clinical features are:
* Typically seen in children
* Deciduous and permanent molars
* Presents as bluish swelling

201
Q

what are the clinical features of a lateral periodontal cyst?

A
  1. Uncommon
  2. Arise adjacent to vital tooth
  3. Canine and premolar region of mandible
  4. Wide age range
  5. Usually symptom-free, incidental finding
  6. Well-circumscribed radiolucency in PDL
202
Q

What is a botryoid odontogenic cyst?

A
  1. Very rare multicystic variant of lateral periodontal cyst
  2. Botryoid= ‘Bunch of grapes’- polycystic appearance
  3. Typically multilocular radiolucency
  4. Mandibular premolar =canine region
  5. Adult
  6. Can recur
203
Q

What is a glandular odontogenic cyst?

A
  1. Very rare
  2. Anterior mandible
  3. Wide age range
  4. Multilocular radiolucency
  5. Strong tendency to recur
204
Q

What is the treatment option for glandular odontogenic cyst?

A

Enucleation but high recurrence rate (up to 50%)

205
Q

What is the treatment option for infant gingival cysts?

A

None usually disappear in a few weeks

206
Q

What is the name of this cyst?

A

Gingival cyst of adult

207
Q

What is the treatment for gingival cysts – adults?

A

Simple excision

208
Q

what is the name of this cyst?

A

Calcifying odontogenic cyst, arising from dental lamina

209
Q

what is the treatment option for calcifying odontogenic cyst?

A

Enucleation, recurrence is rare.

210
Q

There Are two classifications of cysts of the jaw, what are they?

A
  1. Odontogenic – derived from epithelial residues of tooth forming organ (developmental or inflammatory)
  2. Non-Odontogenic – derived from sources other than tooth-forming organ
211
Q

Non-odontogenic cysts are derived from sources other than tooth-forming organs such as:

A
  1. Nasopalatine duct cyst
  2. Surgical ciliated cyst
  3. Nasolabial cyst
212
Q

Where do nasopalatine duct cysts originate from?

A

Originate from epithelium of nasopalatine duct in incisive canal

213
Q

Nasopalatine duct cyst can occur anywhere in the nasopalatine canal, most frequently at which end of the canal?

A

Palatal end

214
Q

Nasopalatine duct cysts can occur at any age but most frequently at which age?

A

5th and 6th decades

215
Q

How fast do nasopalatine cyst grow?

A

They are slow growing appearing as a swelling in midline of anterior palate.

216
Q

What kind of taste can you experience with a nasopalatine cyst?

A

Salty

217
Q

If you took a radiograph of a nasopalatine cyst what would you expect to see?

A

Round or heart-shaped radiolucency in midline of anterior hard palate.

218
Q

Odontogenic and maxillofacial bone tumours WHO classification 2017 include?

A
  1. Odontogenic carcinomas
  2. Odontogenic carcinosarcoma
  3. Odontogenic sarcomas
  4. Benign epithelial odontogenic tumours
  5. Benign mixed epithelial and mesenchymal odontogenic tumours
  6. Benign mesenchymal odontogenic tumours
  7. Odontogenic cysts of inflammatory origin
  8. Odontogenic and non-odontogenic developmental cysts
  9. Malignant maxillofacial bone and cartilage tumours
  10. Benign maxillofacial bone and cartilage tumours
  11. Fibro-osseous and osteochondromatous lesions
  12. Giant cell lesions and bone cysts
  13. Haematolymphoid tumours
219
Q

what are the types of odontogenic carcinomas?

A
  1. Ameloblastic carcinoma
  2. Primary intraosseous squamous cell carcinoma
  3. Sclerosing odontogenic carcinoma
  4. Clear cell odontogenic carcinoma
  5. Ghost cell odontogenic carcinoma
220
Q

Odontogenic carcinosarcoma is a malignant of the epithelial and mesenchymal component, how rare is this?

A

Very rare

221
Q

What are the types of odontogenic sarcomas?

A
  1. Ameloblastic fibrosarcoma
  2. Ameloblastic fibrodentinosarcoma
  3. Ameloblastic fibroodontosarcoma
222
Q

Benign epithelial odontogenic tumours include what?

A
  1. Ameloblastoma
     Ameloblastoma- unicystic type
     Ameloblastoma- extraosseous/peripheral type
     Metastasizing Ameloblastoma
  2. Squamous odontogenic tumour
  3. Calcifying epithelial odontogenic tumour (Pindborg Tumour)
  4. Adenomatoid odontogenic tumour
223
Q

What are the clinical features of ameloblastoma?

A

Clinical features:
1. 2nd most common odontogenic tumour
2. 30-60 yrs
3. Usually posterior mandible
4. Swelling
5. Radiolucent lesion on imaging
6. Slow growing, locally aggressive

224
Q

Histopathology you will see 2 types of tumour cells for ameloblastoma, what are they?

A

2 types of tumour cells
* well-organized peripheral single layer of tall, columnar, pre-ameloblast-like cells, which have nuclei at the opposite pole to the basement membrane (reversed polarity)
* core of loosely arranged cells resembling stellate reticulum

225
Q

Histopathology you will see 2 types of patterns for ameloblastoma, what are they?

A

2 patterns
* follicular (islands of epithelial cells)
* plexiform (long strands of epithelial cells)
Set in fibrous stroma

226
Q

What are the treatment options ameloblastoma?

A
  1. Complete excision with margin of uninvolved tissue
  2. If excision incomplete, it will recur
  3. Longterm follow-up
227
Q

Maxillary ameloblastomas are rare but readily spread through the?

A

thin bones of the base of skull, are difficult to completely excise and are potentially lethal!

228
Q

What are the clinical features of adenomatoid odontogenic tumour?

A

Clinical Features
1. Most in 2nd decade, 90% before 30yrs
2. Females>males
3. Maxilla>mandible
4. Majority in canine region
5. Often associated with unerupted permanent tooth
6. Unilocular radiolucency, may mimic dentigerous cyst
7. Most are asymptomatic

229
Q

What would you expect to see histopathology for adenomatoid odontogenic tumour?

A
  1. Odontogenic epithelium arranged in solid nodules or rosette-like structures
  2. Duct-like structures
  3. Eosinophilic amorphous material
  4. Minimal fibrous stroma
230
Q

What is the treatment plan for adenomatoid odontogenic tumour?

A
  1. Local excision
  2. Recurrence is rare
231
Q

Benign mixed epithelial and mesenchymal odontogenic tumours include what in this category?

A
  1. Ameloblastic fibroma
  2. Primordial odontogenic tumour
  3. Odontoma
  4. odontoma, compound type
  5. odontoma, complex type
  6. Dentinogenic ghost cell tumour
232
Q

What are odontomas?

A

Are developmental malformations (hamartomas) of dental tissues

233
Q

What are the features of odontoma?

A
  1. Once fully calcified do not develop further
  2. Young patients
  3. Painless slow growing lesions
  4. Contain enamel, dentine and sometimes cementum
234
Q

What are the features of odontoma, compound type?

A
  1. Most common odontogenic tumour
  2. Esp Anterior maxilla
  3. Lots of tooth-like structures on imaging
  4. Fibrous capsule enclosing many separate, small, tooth-like structures (denticles/ odontoids)
  5. Aetiology???
235
Q

What are the features of odontoma, complex type?

A
  1. Commonly posterior mandible
  2. Radiopaque mass on imaging
  3. Consist of an irregular mass of hard and soft dental tissues, haphazard arrangement with no resemblance to a tooth and often forming a cauliflower-like mass
  4. Cementum is often very scant
236
Q

What is the treatment option for odontoma?

A
  1. Enucleation
  2. Mature lesions completely enucleated do not recur
  3. Incompletely enucleated developing lesions may recur
237
Q

What types of tumours fall under this category Benign mesenchymal odontogenic tumours?

A
  1. Odontogenic fibroma
  2. Odontogenic myxoma/myxofibroma
  3. Cementoblastoma
  4. Cemento-ossifying fibroma
238
Q

What are clinical features of cementoblastoma?

A
  1. Formation of cementum-like tissue in connection with root of tooth
  2. 10- 40 yrs
  3. Mandible> maxilla, esp associated with 6s
  4. Painful swelling
  5. Tooth remains vital
  6. Well-defined radiopaque or mixed-density lesion
239
Q

What would you expect to see histopathology of cementoblastoma?

A
  1. Dense masses of acellular cementum-like material
  2. Fibrous, sometimes vascular stroma
  3. Tumour blends with root of tooth- helps distinguish lesion from bone tumours
240
Q

What are the treatment of cementoblastoma?

A
  1. Complete excision and removal of tooth
  2. Commonly recur if incompletely excised
241
Q

Odontogenic and maxillofacial bone tumours include?

A
  1. Odontogenic cysts of inflammatory origin
  2. Odontogenic and non-odontogenic developmental cysts
  3. Malignant maxillofacial bone and cartilage tumours
  4. Benign maxillofacial bone and cartilage tumours
  5. Fibro-osseous and osteochondromatous lesions
  6. Giant cell lesions and bone cysts
  7. Haematolymphoid tumours
242
Q

Malignant maxillofacial bone and cartilage tumours

A
  1. Chondrosarcoma- rare
  2. Mesenchymal Chondrosarcoma- very rare
  3. Osteosarcoma- rare
243
Q

Benign maxillofacial bone and cartilage tumours include?

A
  1. Chondroma
  2. Osteoma
  3. Melanotic neuroectodermal tumour of infancy
  4. Chondroblastoma
  5. Chondromyxoid fibroma
  6. Osteoid osteoma
  7. Osteoblastoma
  8. Desmoplastic fibroma
244
Q

What are the features of osteoma?

A
  1. Benign slow-growing tumour consisting of well-differentiated mature bone
  2. Occur mostly in adults, M> F
  3. Mandible>maxilla
  4. Usually solitary lesions, although multiple lesions occur as a feature of Gardner syndrome
  5. Gardner syndrome is rare AD disorder and features include multiple osteomas, polyposis coli (which shows a marked tendency to undergo malignant change), and multiple fibrous tumours and epidermal/sebaceous cysts of skin
245
Q

Histopathology there are two types of osteoma what are they?

A
  1. Compact type- mass of dense lamellar bone with few marrow spaces
  2. Cancellous type- interconnecting trabeculae enclosing fatty or fibrous marrow
246
Q

What are the treatment options for osteoma?

A
  1. Lesions removed if symptomatic or causing problems with fit of denture
  2. Recurrence is rare
247
Q

What are the features for Melanotic Neuroectodermal Tumour of Infancy?

A
  1. Very rare
  2. Most < 1 yr old
  3. M>F
  4. Locally aggressive, rapidly growing pigmented mass
  5. Most frequently anterior maxillary alveolus
248
Q

What would you expect to see histopathology for Melanotic Neuroectodermal Tumour of Infancy?

A
  • Tumour comprises 2 cell population- neuroblastic cells and pigmented epithelial cells
249
Q

What is the treatment options Melanotic Neuroectodermal Tumour of Infancy?

A
  1. Complete local excision is treatment of choice
  2. Most are benign
  3. Can recur
  4. Small number do metastasise
250
Q

Fibro-osseous and osteochondromatous lesions include?

A
  1. Ossifying fibroma
  2. Familial gigantiform cementoma
  3. Fibrous dysplasia
  4. Cemento-osseous dysplasia
  5. Osteochondroma
251
Q

Giant cell lesions and bone cysts include?

A
  1. Central giant cell granuloma
  2. Peripheral giant cell granuloma
  3. Cherubism
  4. Aneurysmal bone cyst
  5. Simple (Solitary) bone cyst
252
Q

What are the features of haematolymphoid tumours?

A
  1. Solitary plasmacytoma of bone
  2. Localized proliferation of monoclonal plasma cells involving bone
  3. Mandible >maxilla
  4. No other bony lesions, no clinical features of plasma cell myeloma
253
Q

what are the clinical features of ossifying fibroma?

A
  1. Slow, painless expansion of bone- jaws and craniofacial skeleton
  2. Peak incidence 3rd- 4th decades
  3. F>M
  4. Different variants- cemento-ossifying fibroma occurs exclusively in the tooth-bearing regions of the jaws
  5. Mandible > maxilla
254
Q

What are the histological features of ossifying fibroma?

A
  1. Well-demarcated or rarely encapsulated benign lesion
  2. Fibrous tissue containing varying amounts of metaplastic bone and mineralised masses resembling cementum
  3. Demarcated nature is an important feature distinguishing it from fibrous dysplasia
255
Q

What is the treatment plan for ossifying fibroma?

A
  1. Complete excision
    * Ossifying Fibroma continues to enlarge if left untreated
    * Must be distinguished from fibrous dysplasia
256
Q

What are the features of familial gigantiform cementoma?

A
  1. Rare form of fibro-osseous lesion of jaws
  2. Early onset of fast growing multifocal/multiquadrant expansive lesions
  3. May be massive with ++ facial deformity
  4. Inheritance in some not all cases
257
Q

What is the treatment plan for familial gigantiform cementoma?

A
  1. Surgery-difficult
258
Q

What are the features of fibrous dysplasia of bone?

A
  1. Fibro-osseous lesion of growing bones
  2. May involve one (monostotic) or several bones (polyostotic)
  3. Sporadic condition
  4. GNAS1 mutations identified
259
Q

What are the features of monostotic fibrous dysplasia?

A
  1. Gives rise to painless bony swelling, facial asymmetry
  2. Usually starts in childhood and arrests in adulthood
  3. M=F
  4. Jaws most frequent head + neck site
  5. Radiographically -orange-peel/ground glass effect
  6. Maxilla>mandible
  7. Maxillary lesions often involve adjacent bones- Craniofacial fibrous dysplasia
260
Q

What are the features of polyostotic fibrous dysplasia?

A
  1. Rare
  2. F>M
  3. Affects several bones
  4. Skin pigmentation and endocrine abnormalities also associated
  5. Albright’s syndrome comprises polyostotic fibrous dysplasia, skin pigmentation and sexual precocity
  6. Head + neck involved in ~50% of cases
261
Q

What are the histological features of polyostotic fibrous dysplasia?

A
  1. Irregularly shaped slender trabeculae of woven (immature) bone lying in a very cellular fibrous tissue
  2. Fuses directly with normal bone at edges of lesion
  3. Lesions stabilise as skeleton matures.
262
Q

What are the treatment options for polyostotic fibrous dysplasia?

A
  • Aesthetic surgery

Rarely, malignant change, typically osteosarcoma, can occur in FD

263
Q

What are the features of cemento-osseous dysplasia?

A
  1. Fibro-osseous lesion occurring in tooth-bearing areas of jaws
  2. Most common fibro-osseous lesion of jaws
  3. Often asymptomatic
  4. Involved teeth remain vital
  5. Characterized by replacement of normal bone by fibrous tissue and metaplastic bone
  6. Predilection for middle-aged African/ African-American females
264
Q

What are the 3 forms of cemento-osseous dysplasia?

A
  1. Periapical cemento-osseous dysplasia
  2. Focal cemento-osseous dysplasia
  3. Florid cemento-osseous dysplasia
265
Q

Periapical cemento-osseous dysplasia involves which region?

A

Involves apical incisor region of mandible, several adjacent teeth involved

266
Q

Focal cemento-osseous dysplasia involves which region?

A

Associated with a single tooth

267
Q

Florid cemento-osseous dysplasia involves which region?

A

Multifocal/multiquadrant

268
Q

What is the treatment option for cemento-osseous dysplasia?

A

Surgery only if symptomatic

269
Q

What are the features of osteochondroma?

A
  1. Bony projection with a cap of cartilage
  2. Continuous with underlying bone
  3. Rare in maxillofacial bones (occurs at sites of endochondral ossification)
  4. Symptoms depend on site of lesion
270
Q

What is the treatment option for osteochondroma?

A

Complete excision

271
Q

What are the categories of giant cell lesions and bone cysts?

A
  1. Central giant cell granuloma
  2. Peripheral giant cell granuloma
  3. Cherubism
  4. Aneurysmal bone cyst
  5. Simple bone cyst
272
Q

What are the features of central giant cell granuloma?

A
  1. Localized benign (but can be aggressive) lesion
  2. Most < 30 years
  3. Mandible > Maxilla
  4. F > M
  5. Often asymptomatic
  6. If cortical plate perforates lesion can present as a peripheral giant-cell granuloma
273
Q

What are the histological features of giant cell granuloma?

A
  1. Large numbers of multi-nucleate, osteoclast-like giant cells
  2. Set in a vascular fibrous stroma
  3. Areas of haemorrhage and haemosiderin
274
Q

What are the features of cherubism?

A
  1. Rare inherited, AD, causing distension of jaws
  2. M>F
  3. Mandible often more extensively involved
  4. Normal at birth but painless swelling, usually bilateral, symmetrical, of jaws appear between 2-4 yrs
  5. Enlarge until ~7yrs
  6. May regress by adulthood
  7. Lesions cause fullness of cheeks and in severe cases maxillary swellings cause eyes to look upward giving ‘Cherub-like” appearance
  8. May be dental anomalies
275
Q

What are the histological features of cherubism?

A
  1. Lesions consist mainly of cellular and vascular fibrous tissue containing varying numbers of multinucleate giant cells
  2. As activity decreases lesions become progressively more fibrous and numbers of giant cells decreases
276
Q

Diagnosis of bone diseases is often difficult and is established by a combination of clinical, radiological, histological and biochemical investigations

Serum levels of calcium, phosphorus and alkaline phosphatase are principal biochemical investigations

A
277
Q

What are the features of osteogenesis imperfecta?

A
  1. Hereditary disease, AD and AR and sporadic
  2. Heterogeneous group of related disorders characterized by impairment of collagen maturation
  3. Collagen is component of bone, ligaments, sclerae, dentine, skin
  4. Several different types of OI, type I most common and mild
278
Q

Variety of clinical features:

A
  1. Easily fractured, osteoporotic bone
  2. Affected teeth appear as in dentinogenesis imperfecta
  3. Malocclusion may be a problem
279
Q

What are the features of osteopetrosis (marble bone disease)

A
  1. Group of rare genetic diseases in which there is marked increase in bone density- infantile and adult forms
  2. Due to failure of normal osteoclast activity and absence of normal modelling resorption
  3. Cortices are thickened and sclerosis of cancellous bone
  4. Anaemia is common due to marrow space deficiency
  5. Osteomyelitis is a recognized complication and prevention of dental infections important
280
Q

What are the features of cleidocranial dysplasia?

A
  1. Rare genetic disorder, AD and sporadic
  2. Characterized by abnormalities of many bones but most notably there is defective formation of the clavicles, delayed closure of fontanelles and sometimes retrusion of the maxilla
  3. Partial or complete absence of clavicles allows patient to bring shoulders together in front of the chest
  4. Dental anomalies are common, particularly delayed eruption of permanent dentition and supernumerary teeth (often numerous)
  5. Narrow, high-arched palate
281
Q

What are the features of achondroplasia?

A
  1. May be AD inheritance or spontaneous
  2. Associated with an abnormality in endochondral ossification
  3. Head and trunk of normal size but limbs are excessively short
  4. Defective growth at base of skull leads to a retrusive maxilla, often resulting in severe malocclusion
282
Q

What are the features of osteoporosis?

A
  1. Results when bone loss is excessive or when apposition of bone is reduced
  2. Most common in postmenopausal women
  3. Also accentuated in other diseases including Cushing syndrome, thyrotoxicosis and primary hyperparathyroidism
  4. Osteoporotic bone is of normal composition but is reduced in quantity
  5. There is increased radiolucency of bone, cortex is thinned, and there are more marrow spaces in the cancellous bone associated with thin trabeculae
  6. Both jaws may be affected
  7. Nb Bisphosphonates
283
Q

What are the features of hyperparathyroidism?

A
  1. Overproduction of parathormone, PTH
  2. Mobilises calcium and raises the plasma calcium level
  3. Primary hyperparathyroidism usually due to hyperplasia or adenoma of the parathyroids
  4. Most patients are female and postmenopausal
  5. Secondary hyperparathyroidism develops when PTH produced in response to chronic low calcium levels, often seen in chronic renal disease
  6. Patients present with ‘stones, bones and abdominal groans’
  7. Stones- renal calculi and other calcifications
  8. Bones- various bone lesions including ‘brown tumour’ of hyperparathyroidism
  9. Abdominal groans- tendency to develop duodenal ulcers
  10. May present in dental patients as a cyst-like swelling of the jaw which displays the histological features of a giant-cell lesion
284
Q

What are the histological features of hyperparathyroidism?

A

Histologically it is impossible to distinguish ‘brown tumour’ of hyperparathyroidism from other giant-cell lesions of bone (central giant cell granuloma, aneurysmal bone cyst) therefore clinical, radiological and biochemical investigations required

285
Q

What are the features of rickets and osteomalacia?

A
  1. Rickets and its adult counterpart osteomalacia are due to deficiency of, or resistance to the action of, vitamin D
  2. Failure of mineralization of osteoid and cartilage
  3. Dental defects rarely seen except in very severe cases when hypocalcification of dentine and enamel hypoplasia may occur
  4. May also be a delay in tooth eruption
  5. Dental defects also seen in hypophosphataemia (Vitamin-D resistant rickets)
286
Q

What are the features of acromegaly?

A
  1. Caused by prolonged and excessive secretion of growth hormone
  2. Usually due to anterior pituitary tumour developing after epiphyses have closed
  3. There is renewed growth of the bones of the jaws, hands and feet with soft tissue overgrowth also
  4. Activation of condylar growth centre of mandible causes jaw to become enlarged and protrusive with increased spacing between teeth
  5. Thickening of facial soft tissues
287
Q

What are the features of inflammatory disease of bone alveolar osteitis (dry socket)

A
  1. Unpredictable complication of extractions, particularly lower molars
  2. Due to failure of blood clot to form or dislodgment or breakdown of clot.
  3. Bone of socket becomes infected and necrotic and very painful!
  4. Inflammatory reaction in adjacent marrow localises the infection to the walls of the socket, otherwise osteomyelitis would ensue
  5. Dead bone is separated by osteoclasts and small sequestra form and are shed
288
Q

What are the features of osteomyelitis?

A
  1. Spectrum of inflammatory and reactive changes in bone and periosteum
  2. Typically in mandible of adults
  3. Reflects a balance between the nature and severity of the irritant, the host defences, and local and systemic predisposing factors
  4. Acute and chronic suppurative and non-suppurative and sclerotic forms
289
Q

What are the features of radiation injury and osteoradionecrosis?

A
  1. Radiation affects the vascularity of bone by causing proliferation of the intima of the blood vessels (endarteritis obliterans)
  2. Potentially serious in mandible with its end artery supply
  3. ID artery or its branches may become thrombosed
  4. The non-vital bone which results is sterile and asymptomatic but very susceptible to infection and trauma
  5. Infection can spread rapidly through irradiated bone, resulting in extensive osteomyelitis and painful necrosis of bone
  6. Can be very difficult to treat
290
Q

What are the features of medicine-related osteonecrosis of the jaws (MRONJ)

A
  1. Bisphosphonates are a class of drugs that inhibits osteoclasts
  2. Used in some cancers, Paget’s disease of bone and osteoporosis
  3. Anti-angiogenic drugs target the processes by which new blood vessels are formed and are used in cancer treatment to restrict vascularisation of tumours
  4. MRONJ defined as’ exposed bone, or bone that can be probed through an intraoral or extraoral fistula, in the maxillofacial region that has persisted for more than eight weeks in patients with a history of treatment with anti-resorptive or anti-angiogenic drugs, and where there has been no history of radiation therapy to the jaw or no obvious metastatic disease to the jaws’
  5. Various associated risk factors including high dose, IV administration, etc
  6. Symptoms include delayed healing following a dental extraction or other oral surgery, pain, soft tissue infection and swelling, numbness, paraesthesia or exposed bone
  7. Osteonecrosis may be spontaneous or follow invasive dental procedure
  8. Histologically fragments of non-vital bone often with prominent bacterial colonization
  9. Refer to current guidelines for management
291
Q

What are the features of Paget’s disease of bone (osteitis deformans)?

A
  1. Form of osteodystrophy characterised by disorganised formation and remodelling of bone unrelated to functional requirements
  2. Aetiology unknown ?? Paramyxovirus ??Genetic Factors ? endocrine
  3. Relatively common
  4. Often subclinical
  5. 40yrs
  6. ?M>F
  7. Geographic variation in incidence
  8. Chronic slowly progressing condition
  9. Single or multiple bones can be affected
  10. Sacrum, spine, skull, femora and pelvis most common sites
  11. Can be asymptomatic or be painful
  12. Maxilla more often affected than mandible
  13. Patients show varying degrees of bony deformation and distortion of weight-bearing portions of skeleton
  14. Affected bones are thickened but weaker and pathological fractures occur
  15. Progressive enlargement of skull and facial bones- hats don’t fit, dentures don’t fit
  16. Narrowing of foramina can cause cranial nerve deficits
  17. In dentate, derangement of occlusion and spacing of the teeth can occur
  18. Also may be hypercementosis and ankylosis of teeth leading to extraction difficulties
  19. Development of osteosarcoma is a recognised, rare complication of Paget’s disease of bone
  20. Giant cell tumours may also arise in bones affected by Paget’s
  21. Characteristic radiographic ‘cotton-wool’ appearance
292
Q

What are the progressive and overlapping phases of Paget’s disease of bone?

A
  1. Initial predominately osteolytic phase
  2. Active stage of mixed osteolysis and osteogenesis
  3. Predominately osteoblastic or sclerotic phase
293
Q

What are the histological features of Paget’s disease? –

A

varies with phase

  • Main features are irregular pattern of reversal lines, many osteoblasts and osteoclasts, fibrosis of marrow spaces and increased vascularity
  • Destruction and new bone formation may alternate rapidly, marked histologically by haemotoxylin-staining reversal lines Their irregular pattern produces a ‘Mosaic’ appearance in the bone
  • Early phase there is typically more resorption than osteoblastic activity
  • Late stage bones are thick, cortex and medulla are obliterated and the whole bone is spongy in texture
294
Q

What are the treatment options for Paget’s disease of bone?

A
  1. Calcitonin
  2. Bisphosphonates (nb MRONJ!)
295
Q

What are the features of torus palatinus, torus mandibularis and other exostoses?

A
  1. Exostoses are localised bony protuberances
  2. Non-neoplastic lesion that may be developmental in origin or may be a response to a stimulus such as chronic trauma
  3. A torus is an exostosis which occurs at a characteristic site, either in the midline of the palate (torus palatinus) or on the lingual surface of the mandible, usually premolar region above the mylohyoid line (torus mandibularis)
  4. Mandibular tori often bilateral
  5. Typically seen in adults
  6. Their aetiology is unknown
  7. Exostosis may be composed entirely of dense, cortical bone or consist of cancellous bone with a shell of cortical bone
  8. Entirely benign
  9. Exostoses are occasionally seen elsewhere in the mouth and may be multiple esp buccal alveolus in molar region of the maxilla
  10. Distinction between exostosis and osteoma often difficult to determine
  11. May cause problems with dentures
296
Q

What is the pathology of the TMJ?

A

Classification of TMJ disorders includes:
1. Developmental anomalies (e.g. condylar hyperplasia, hypoplasia, aplasia)
2. Osteoarthrosis
3. Rheumatoid arthritis
4. Inflammatory arthritis (e.g. psoriasis, systemic lupus erythematosus)
5. Infective arthritis (local or systemic)
6. Neoplasia
7. Metabolic disease (e.g. gout, chondrocalcinosis)
8. Synovial disease (e.g. Pigmented Villonodular Synovitis)
9. Miscellaneous conditions (e.g. Paget’s disease of bone, acromegaly)

dentistry year 4: module 7 (10 decks)

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