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Lumps, Bumps & Pigmented Things

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Presentation on theme: "Lumps, Bumps & Pigmented Things"— Presentation transcript:

1 Lumps, Bumps & Pigmented Things
By Iain Macleod

2 Assessment of a lump Site Size Shape Surface Colour Consistency Edge
Solitary or Multiple

3 Differential diagnosis of a lump
Hyperplasia vs Neoplasia Neoplastic Benign vs Malignant Wide differential diagnosis

4 Common clinically benign lumps
Fibroepithelial polyp Pyogenic granuloma Epulides Denture granuloma Squamous cell papilloma Mucoceles

5 FORDYCE DISEASE (Fordyce Granules)
Yellowish Plaques or Papules Usually Multiple and Bilateral Usually Buccal Mucosa (but may be found anywhere) Ectopic Sebaceous Glands Common (~80%) No treatment required - clinical diagnosis

6 FOLIATE PAPILLAE (Lingual Tonsil??)
Normal Anatomic Structures Posterior Lateral Tongue Tissue Swelling with Vertical Grooves Containing Taste Buds and von Ebner Salivary Glands Often Include Hyperplastic Lymphoid Aggregate No Treatment Required - May require biopsy for diagnosis

7 LYMPHOID AGGREGATES Small “Reddish-Yellow” Nodules / Papules
Soft Palate or Base of Tongue (Lingual Tonsils) Part of Waldeyer’s Ring “Ectopic” Lymphoid Tissue No treatment required - may require biopsy for diagnosis


9 Vascular anomalies Hamartomas – Benign neoplasms Haemangioma
Lymphangioma Sturge – Weber syndrome (encephalofacial angiomatosis) Malignant variants – eg. Kaposi’s sarcoma Varicosities / venous lakes

10 VARICOSITIES Reddish-Blue to Purple Nodules (Usually < 5 mm.) - Dilated Veins Lip, Buccal Mucosa, Ventral/Lateral Tongue, Floor of Mouth Age Associated (more common in older patients) Will Blanch on pressure No treatment required - May require biopsy for diagnosis


12 Connective tissue hyperplasias
Epulides (epulis) Denture irritation hyperplasia Papillary hyperplasia of palate Fibroepithelial polyp Fibrous tuberosities Chronic hyperplastic gingivitis Drug induced gingival hyperplasias

13 Epulides Fibrous Vascular – pyogenic granuloma , pregnancy epulis
Giant cell – peripheral , central , hyperparathyroidism (raised PTH , calcium) Congenital

14 Giant cell granuloma Peripheral Central Radiographs
Hyperparathyroidism Check blood chemistry – calcium & PTH levels

15 Gingival fibrous hyperplasia
Familial Drug induced – eg.phenytoin, cyclosporin , nifedepine Pubertal

16 Salivary Gland Swellings

17 Salivary Disorders Developmental Obstructive Infectious Autoimmune

18 Obstructive Salivary Diseases
Mucous Extravasation (Mucocele) Ranula Sialolithiasis Ductal Compression (Tumours)

19 Mucous Retention (Extravasation)
Lower lip>Buccal mucosa>Ventral tongue Trauma, ductal laceration Mucous escape into connective tissue Walling-off effect Excision, extirpation of feeder glands

20 Sialolithiasis SMG>Parotid>Minor Glands Pain at mealtimes
Glandular tender swelling Negative secretion upon milking Occlusal and other radiographs

21 Sialadenitis Endemic Parotitis (Mumps)
Sclerosing, secondary to duct blockage Bacterial Sialadenitis Autoimmune Sialadenitis

22 Sialosis (sialadenosiss)
Idiopathic enlargement of salivary glands – most often parotids Metabolic factors Alcohol Drugs Diabetes Anorexia & bulimia

23 Necrotizing Sialometaplasia
Ulcerative Lesion Non-elevated margins with necrotic centre Palate most common site Often Painless Necrosis of acini Ducts undergo squamous metaplasia

24 Salivary Gland Neoplasia

25 Classification – WHO (modified)
Adenomas Pleomorphic adenoma Warthin tumour (adenolymphoma) Basal cell adenoma Oncocytoma Canalicular adenoma Ductal papillomas Carcinomas Mucoepidermoid carcinoma Acinic cell carcinoma Adenoid cystic carcinoma Carcinoma arising in pleomorphic adenoma Polymorphous low grade adenocarcinoma Other carcinomas

26 Salivary Neoplasms Rule of nines: 9/10 are benign; 9/10 occur in parotid; 9/10 are pleomorphic adenomas Look for rate of growth Parotid – facial nerve involvement – highly suggestive of malignancy Most painless but adenoid cystic carcinoma spreads perineurally – painful!

27 Rule of thumb!------ Swellings in lower lip – mucoceles; swellings in upper lip - neoplasms

28 Facial Palsy Upper motor neurone - Spares forehead
Lower motor neurone – complete palsy

29 Bone lumps

30 TORI (plural) / TORUS (singular) Palatal or Mandibular
Bony Growths Mid-Hard Palate (20%) Lingual Mandible (10%) May show up as X-Ray Radiopacity Anywhere else called “Exostoses” subject to trauma and ulceration No Treatment Required (unless necessary for Denture construction)

31 Pigmentation

32 Definitions Endogenous: the source of pigment is from inside the body
Haemoglobin  red / blue Haemosiderin  brown Melanin  brown Overproduction Overpopulation Exogenous: the source of the pigment is from outside the body Traumatic deposition (amalgam / graphite tattoo) Ingested heavy metals Colonization of bacteria (hairy tongue)

33 Classification of pigmented lesions:
Blue/purple vascular lesions Brown melanotic lesions Brown Haem-associated lesions Grey/black pigmentations

34 I- Blue/purple vascular lesions
Haemangioma Varix Angiosarcoma Kaposi’s sarcoma Hereditary Haemorrhagic Talangiectasia (HHT)

35 Hereditary Haemorrhagic Talangiectasia (HHT)
Microaneurysms caused by weakening defect in the adventitial coat of venules Genetic disease (autosomal dominant) Multiple round/oval purple papules <0.5 cm >100 lesions oral and nasal mucosa Facial skin and neck may also be affected Diagnosis: Family history Epistaxis which might be severe Platelet studies are normal More purple and nodular not macular like petechiae No treatment

36 Brown melanotic lesions
Physiologic pigmentations Smoker’s melanosis Ephilis and oral melanotic macule Naevocellular nevus and blue nevus Malignant melanoma Drug-induced melanosis Café-au lait pigmentation Pigmented lichen planus Endocrinopathic pigmentation HIV oral melanosis Peutz-jeghers syndrome

37 Ephelis and oral melanotic macule
Ephelis in skin and intra-oral melanotic macule in mucosa oval / irregular in outline, brown or black Don’t enlarge if they reach a certain size Overproduction of melanin confined to the basal cell layer or the immediately adjacent keratinocytes Have no malignant transformation risk Surgical excision and review

38 Naevus Naevi results from benign proliferations of melanocytes
When a meloncyte mature it becomes a naevus cell Two types: Naevocellular naevi Blue naevi common on the skin but rare in the oral mucosa A nevus cell is a physiologic relative of the melanocyte which lacks dendrites, oval shape and has a tendency to nest

39 Naevocellular naevus JUNCTIONAL NAEVUS
Focal proliferation of melanocytes in the basal layer  clinically appear as round or oval melanotic macule COMPOUND NAEVUS contains groups of naevus cells in the connective tissue Some cells remain in contact with the basal keratinocytes  clinically appear as dome shaped nevus INTRAMUCOSAL / INTRADERMAL NAEVUS: located entirely within the lamina propria. Clinically in skin appear as nodule with few hairs often protruding

40 Blue naevus Form ~ 1/3 of all oral naevi
Located deeper than intramucosal naevi  blue color Characterized by a proliferation of spindle-shaped pigmented melanocytes and melanophages loosely grouped together

41 Look for: Asymmetry, Irregular border, Colour, Change in size
Moles! Look for: Asymmetry, Irregular border, Colour, Change in size Bleeding or Itchiness

42 Malignant melanoma Rare
Arises from neoplastic transformation of either melanocytes or naevus cells Aetiology of oral melanoma is unknown Peak incidence years Lesions typically dark brown/bluish black/ mixture of colours or rarely non-pigmented (red) Starts as asymptomatic macule of irregular margins (months/years) then become slightly raised or nodular Ulceration, pain, bleeding, loosening of teeth may present

43 Malignant melanoma Metastases are common with spread to regional lymph nodes, lungs, liver, brain and bones 5 year survival rate is only 5% in patients who present with cervical lymph node metastases Tumour thickness is the single most important prognostic feature HISTOPATHOLOGY: malignant melanocytes invading both epithelium and connective tissue

44 Drug-induced melanosis
Large multifocal melanotic macule (no nodularity/swellings) Increase in melanin pigmentation NOT in number of melanocytes Pigmentation remains some time after stopping medication Examples: Minocycline Anti-malarials Zidovudine (AZT) Oral contraceptives Cytotoxics Anti-convulsants (phenothiazines) AZT: nucleoside reverse transcriptase inhibitor antiviral agent used to treat human immunodeficiency virus (HIV) infection Minocycline: It is primarily used to treat acne and other skin infections as well as lyme disease as the one pill twice daily 100 mg dosage is far easier for patients than the four times a day required with tetracycline or oxytetracycline.

45 Pigmented lichen planus
Rarely erosive OLP can be associated with diffuse melanosis This can be related to the T cell infiltration and basal cell layer degeneration Histologically: the usual features of OLP are observed along with basilar melanosis and melanin incontinence.

46 Endocrinopathic pigmentation
ADDISONS DISEASE: Cortisol  ACTH & Melanin Stimulating Hormone (MSH) diffuse cutaneous pigmentation and multiple oral melanotic macules PITUITARY GLAND BASED CUSHING’S DISEASE: adenoma in the pituitary gland ACTH & MSH

47 HIV oral melanosis Aetiology remains undetermined
Could not be related to adrenocortical involvement or medications affect skin, nails and mucous membrane (Buccal mucosa most commonly affected)

48 Peutz-jeghers syndrome
Autosomal dominant inheritance Multiple peri-oral epelides less than 0.5 cm in diameter. Similar lesions may occur on the tongue, buccal mucosa and labial mucosa Intestinal polyposis: This is low possibility for malignant transformation

49 Albrights Syndrome Polyostotic fibrous dysplasia precocious puberty
other endocrine abnormalities Skin pigmentation frequently overlies affected bones pigmentation of oral mucosa is rare

50 Brown Haem-associated lesions
Ecchymosis Petechia Haemochromatosis

51 Ecchymosis Common on the face and lips but not intraorally
Immediately after the trauma it will appear as a red macule or a swelling, after few days it becomes brown (hemoglobin degraded to haemosiderin) Ecchymosis can be seen in Patients taking anticoagulant drugs Chronic liver failure

52 Petechia Generalized if secondary to platelet deficiencies or aggregation disorder Idiopathic thrombocytopenic purpura (ITP) HIV- related ITP Aspirin toxicity Bone marrow suppression by chemotherapy Localized to soft palate Excessive suction to relieve pruritus caused by common cold or allergy

53 Haemochromatosis Iron overload leading to deposition of haemosiderin pigment in multiple organs Primary heritable disease with a prominent male predilection Can be secondary to chronic anaemia, cirrhosis, or excess intake of iron Brown to grey diffuse macules that tend to occur on the palate and gingiva

54 Grey/black pigmentations
Amalgam tattoo Graphite tattoo Hairy tongue Pigmentation related to heavy-metal ingestion

55 Pigmentation related to heavy-metal ingestion
Now is rare Heavy metals ingestion caused by: Medication Occupational (industry & paint) Deposited in skin and oral mucosa Typically linear distribution in gingivae Can also get systemic toxicity (behavioural changes & neurological disorders)

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