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 “ReddishYellow” 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
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
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 Gland Swellings
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
Salivary Gland Neoplasia
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
Bone lumps
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)
Pigmentation
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:
1. Blue/purple vascular lesions
2. Brown melanotic lesions
3. Brown Haem-associated lesions
4. 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
1. Physiologic pigmentations
2. Smoker’s melanosis
3. Ephilis and oral melanotic macule
4. Naevocellular nevus and blue nevus
5. Malignant melanoma
6. Drug-induced melanosis
7. Café-au lait pigmentation
8. Pigmented lichen planus
9. Endocrinopathic pigmentation
10. HIV oral melanosis
11. 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:
1. Minocycline
2. Anti-malarials
3. Zidovudine (AZT)
4. Oral contraceptives
5. Cytotoxics
6. 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
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
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
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
Grey/black pigmentations
•
•
•
•
Amalgam tattoo
Graphite tattoo
Hairy tongue
Pigmentation related to heavy-metal
ingestion
Pigmentation related to heavymetal 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)