1. Lumps, Bumps & Pigmented ThingsBy
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 TISSUE HYPERPLASIAS

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
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)