Lumps, Bumps & Pigmented Things

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

8. VASCULAR ANOMALIES

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

11. CONNECTIVE TISSUEHYPERPLASIAS

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 • Neoplastic

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

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. 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 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

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)

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