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Lumps, Bumps & Pigmented Things. By Iain Macleod. Assessment of a lump. Site Size Shape Surface Colour Consistency Edge Solitary or Multiple. Differential diagnosis of a lump. Hyperplasia vs Neoplasia Neoplastic Benign vs Malignant Wide differential diagnosis.
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Lumps, Bumps & Pigmented Things By Iain Macleod
Assessment of a lump Site Size Shape Surface Colour Consistency Edge Solitary or Multiple
Differential diagnosis of a lump Hyperplasia vs Neoplasia Neoplastic Benign vs Malignant Wide differential diagnosis
Common clinically benign lumps Fibroepithelial polyp Pyogenic granuloma Epulides Denture granuloma Squamous cell papilloma Mucoceles
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
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
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
Vascular anomalies • Hamartomas – Benign neoplasms • Haemangioma • Lymphangioma • Sturge – Weber syndrome (encephalofacial angiomatosis) • Malignant variants – eg. Kaposi’s sarcoma • Varicosities / venous lakes
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
Connective tissue hyperplasias • Epulides (epulis) • Denture irritation hyperplasia • Papillary hyperplasia of palate • Fibroepithelial polyp • Fibrous tuberosities • Chronic hyperplastic gingivitis • Drug induced gingival hyperplasias
Epulides • Fibrous • Vascular – pyogenic granuloma ,pregnancy epulis • Giant cell – peripheral , central ,hyperparathyroidism (raised PTH ,calcium) • Congenital
Giant cell granuloma • Peripheral • Central • Radiographs • Hyperparathyroidism • Check blood chemistry – calcium & PTH levels
Gingival fibrous hyperplasia • Familial • Drug induced – eg.phenytoin, cyclosporin , nifedepine • Pubertal
Salivary Disorders • Developmental • Obstructive • Infectious • Autoimmune • Neoplastic
Obstructive Salivary Diseases • Mucous Extravasation (Mucocele) • Ranula • Sialolithiasis • Ductal Compression (Tumours)
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
Sialolithiasis • SMG>Parotid>Minor Glands • Pain at mealtimes • Glandular tender swelling • Negative secretion upon milking • Occlusal and other radiographs
Sialadenitis • Endemic Parotitis (Mumps) • Sclerosing, secondary to duct blockage • Bacterial Sialadenitis • Autoimmune Sialadenitis
Sialosis (sialadenosiss) • Idiopathic enlargement of salivary glands – most often parotids • Metabolic factors • Alcohol • Drugs • Diabetes • Anorexia & bulimia
Necrotizing Sialometaplasia • Ulcerative Lesion • Non-elevated margins with necrotic centre • Palate most common site • Often Painless • Necrosis of acini • Ducts undergo squamous metaplasia
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
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!
Rule of thumb!------ • Swellings in lower lip – mucoceles; swellings in upper lip - neoplasms
Facial Palsy • Upper motor neurone - Spares forehead • Lower motor neurone – complete palsy
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)
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)
Classification of pigmented lesions: • Blue/purple vascular lesions • Brown melanotic lesions • Brown Haem-associated lesions • Grey/black pigmentations
I- Blue/purple vascular lesions • Haemangioma • Varix • Angiosarcoma • Kaposi’s sarcoma • Hereditary Haemorrhagic Talangiectasia (HHT)
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
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
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
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
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
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
Moles! Look for: Asymmetry, Irregular border, Colour, Change in size Bleeding or Itchiness
Malignant melanoma • Rare • Arises from neoplastic transformation of either melanocytes or naevus cells • Aetiology of oral melanoma is unknown • Peak incidence 40-60 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
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
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)
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.
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
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)
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
Albrights Syndrome • Polyostotic fibrous dysplasia • precocious puberty • other endocrine abnormalities • Skin pigmentation frequently overlies affected bones • pigmentation of oral mucosa is rare
Brown Haem-associated lesions • Ecchymosis • Petechia • Haemochromatosis