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TEMPOROMANDIBULAR JOINT DISORDERS

Diagnosis is aided with OPG, and isotope bone scans can also be useful. Management is with removal of the growth plate, and when burnt out, orthognathic jaw realignment.

Infection of the TMJ

Infection of the TMJ is an uncommon occurrence in the developed world. It can be due to direct inoculation of the joint or distant spread. Primary infection can be bony (osteomyelitis) or involve the so tissue (arthritis). e usual causative agent is Staphylococcus aureus. e most common cause is local spread from neighbouring structures—ear, brain, or oropharynx. Haematogenous spread is rare.

Management includes diagnostic aspiration, intravenous antibiotics, and systemic support if required. Repeated arthrocentesis may be required.

Neoplastic Disease of the TMJ

Primary benign and malignant tumours of the TMJ are rare and include chondroma, osteochondroma, and osteoma. Benign tumours tend to have slow growth and present with occlusal deformity, centreline deviation, and chin point changes.

Management includes excision and reconstruction, with or without orthognathic corrective surger y.

Iatrogenic/Idiopathic Disorders

e previous use of open surgery for pain, restriction, and joint noises has led to troublesome sequelae. Most of the problems include pain from local damage and are best managed in conjunction with the pain team.

Initial Management

e primary management of most TMJ disorders is reassurance that there is unlikely to be a signicant underlying condition. e disorder is unlikely to precede arthritis, and the majority of patients can be managed with nonsurgical treatments. ere is an underlying psychological component in a signicant number of patients.

Explanation of the disease process will help empower the patient and reduces the risk of the patient’s following misleading advice found on the internet.

Initial resting of the joint, with avoidance of sticky foods and restriction of wide mouth opening, will gradually improve most symptoms over a period of weeks. Use of a topical NSAID will give additional benet.

A lower, so, full occlusal coverage splint to wear at night helps reduce load on muscles and joint overnight and gives particular benet to those with a clenching habit. Again, it takes several weeks for the benet to be felt.

Following a 2-month trial, if there has been no signicant improvement or if there is severe restriction, then referral to a specialist is warranted.

Referral for maxillofacial advice is indicated when there is:

Acute severe restriction of opening

•

Failure of conservative measures in conjunction with dental care over 2 months

•

Associated rheumatological disease

•

Recurrent dislocation of joint

•

Disturbance of dental occlusion

•

Surgical Management

Surgery can be divided into open and closed procedures. Closed procedures are arthrocentesis and arthroscopy. Arthrocentesis is the washing out of the upper joint space with 200 ml of isotonic solution, most commonly under general anaesthesia. It gives 70–80% improvement in cases of locking, restriction, and pain. Arthroscopy is similar but allows visualisation of the interna l joint anatomy. Both procedures ca rry a 1% risk of temporar y temporal branch wea kness.

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Open joint surgery is approached by a pre-auricular incision, avoiding the facial nerve. Procedures include eminoplasty (modication of the articular eminence), condylar shave (modication of the condylar head), and full joint replacement. For full joint replacement, outcomes of >90% joint survival have been reported at 15 years.

Conclusion

TMJ disorders are a common cause of morbidity, although most can be managed with simple measures. Surgery should be considered a last resort.

Further Reading

1. Rajapakse S, Ahmed N, Sidebottom AJ. Current thinking about the management of dysfunction of the temporomandibular joint: a review. Br J Oral Maxillofacial Surg 2017; May (4): 351–356.

2. Connelly ST, Tartaglia G, Silva RG. (Eds.) Contemporary Management of Temporomandibular Disorders, 2019. ISBN 978-3-030-13328-3.

3. National Institute of Health and Care Excellence Guidelines: Temporomandibular Disorders (TMDs). (Last revised December 2016.)

76. BENIGN AND MALIGNANT CONDITIONS OF THE SKIN

Introduction

One in every three cancers is a skin cancer.

Common or important benign and malignant skin lesions that are discussed here are shown in bold in Table 76.1.

Benign and Premalignant Skin Lesions

Actinic Keratosis (AK)

Actinic keratosis is the most common premalignant lesion, with a low transformation rate into SCC. Found on sun-exposed areas (80% occur on the head and neck or hands). Asymptomatic, palpable, dry, scaly lesions. Biopsy is indicated if SCC is suspected. Nonsurgical options include topical treatments (e.g. 5-uorouracil or imiquimod), cryotherapy, or photodynamic therapy (PDT). Surgery is either curettage and cautery (C&C) or excision with 2-mm margins.

Bowen’s Disease (BD; A.K.A. Squamous Cell Carcinoma in situ)

Risk of progression to SCC is 3–5%. Occurs on sun-exposed areas (mainly head and neck and lower limb). Lesions are asymptomatic, long-standing, and slow-growing well-dened/ demarcated scaly er ythematous plaques . Biopsy excludes dierentials (e.g. SCC). Nonsurgical and surgical management are similar to those for AK.

Keratoacanthoma (KA)

KA clinically and histologically resembles well-dierentiated SCC. However, it enlarges rapidly over 6 weeks and then regresses. Management is either observation (because KA spontaneously involutes) or removal if there is concern about SCC. Associations include Ferguson-Smith and Muir-Torre syndromes.

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BENIGN AND MALIGNANT CONDITIONS OF THE SKIN

Table 76.1 Examples of skin lesions

Main classication Subclassication Examples

Benign nonpigmented Epidermal Actinic keratosis, Bowen’s disease,

keratoacanthoma, keratin horn, viral

wart, squamous papilloma, seborrheic keratosis

Dermal Hair follicle: Trichoepithelioma,

pilomatrixoma Sebaceous gland: Sebaceous naevus Sweat gland: Cylindroma Neural tissue: Neurobroma Miscellaneous: Cysts (e.g. dermoid)

Malignant nonpigmented Common Basal cell carcinoma (BCC), squamous cell

carcinoma (SCC)

Uncommon Merkel cell carcinoma, sebaceous

carcinoma

Benign pigmented Naevus cell naevi Congenital—Congenital melanocytic naevus

Acquired—Junction naevus, compound

naevus, intradermal naevus Special—Spitz naevus, spindle cell nevus,

halo naevus

Melanocytic naevi Epidermal—Ephelis (freckle), lentigo,

café-au-lait spot Dermal—Blue naevus

Premalignant pigmented Dysplastic/atypical mole

Lentigo maligna/melanoma in situ

Malignant pigmented Melanoma Soft tissue tumours Cutaneous sarcoma DFSP, MFX, AFX

Dysplastic/Atypical NevI

Dysplastic/atypical naevi occur in 5% of the population. ey contain atypical melanocytes but no invasion. ere is a 5% risk of change to melanoma. ey have unusual features: >5 mm diameter, irregular border, and pigment. FAMM syndrome (high risk of melanoma) is >50 moles, dysplastic on histology, and a 1st/2nd-degree relative with melanoma. Management is in an atypical mole clinic and includes full skin examination with dermatoscopy and photographs. If there is diagnostic uncertainty, then treatment is excision with 2-mm margins.

Lentigo and Lentigo Maligna/Melanoma in situ

Lentigo is an increased number of normal melanocytes, lentigo maligna is an increased number of abnormal melanocytes, and lentigo maligna melanoma is invasive. Assessment of lentigo is with dermatoscopy, and if there is diagnostic uncertainty, then treatment is excision. Lentigo maligna/melanoma in situ is managed by excision with 5 mm margins, although histology may show incomplete margins, as associated with ‘eld change,’ and therefore require post-excision imiquimod or observation.

Non-Melanoma Skin Cancers (NMSC)

BCC and SCC are the main types.

Risk Factors

Risk factors are shown in Tables 76.2 and 76.3. Fitzpatrick types 1 and 2 have the highest risk.

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Table 76.2 Risk factors for non-melanoma skin cancers

Risk factor Examples

Radiation Chronic sun exposure (e.g. UVA/B), ionising radiation Premalignant conditions AK, BD, KA, keratin horn, viral infection (e.g. HPV-related SCC),

sebaceous naevus Chronic wounds Marjolin’s ulcer (SCC) Immunosuppression Malignancy, drugs Toxins Smoking (SCC lip), soot, arsenic Genetics Xeroderma pigmentosum, albinism, Gorlin’s syndrome (BCC)

Table 76.3 Fitzpatrick skin types

Type Colour and response to sunlight

1 Pale white, never tan, and always burn 2 Fair skin, difcult tan, and usually burn 3 Light brown, gradual tan, and sometimes burn 4 Mediterranean, easy tan, and minimal burn 5 Indian, very easy tan, and rarely burn 6 Black, never burn

Staging

Points on BCC/SCC American Joint Committee on Cancer (AJCC) 8th edition TNM classication:

a. Tumuor (T): T1 <2 cm, T2 2–4 cm, T3 > 4 cm or deep (e.g. >6 mm, perineural invasion,

beyond fat or minor bone), T4a gross bone involvement, and T4b skull base involved.

b. Node (N): Specic category for head and neck. c. Staging: Stage 1 = T1, Stage 2 = T2, Stage 3 = T3 or T1–3N1, Stage 4a = T4, T1–3N2/3,

Stage 4b = M1.

Basal Cell Carcinoma

Background

75% of NMSC. From epidermal keratinocytes. Locally invasive. Distant metastases are rare.

Clinical Features

Slow growing over months/years. Classically, pearly appearance with telangiectasia.

Classied as nodular (75%), supercial (15%), inltrative/morpheaform (10%), other.

Diagnosis

Clinical, but punch biopsy to exclude dierentials. Imaging (e.g. CT/MRI) if deep invasion.

Management

Principles

Decide if ‘high risk’ or ‘xed’. Risk factors: Macroscopic—Increasing size, poorly dened, location on central face. Microscopic—Inltrative/morpheaform or perineural invasion. Systemic—Immunosuppression.

Nonsurgical

Supercial BCC: Topical treatment (e.g. imiquimod/5-uorouracil), PDT, or cryotherapy.

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BENIGN AND MALIGNANT CONDITIONS OF THE SKIN

Surgical

Options include:

1 Destructive treatments if small, well-dema rcated/supercial: C&C, cr yotherapy, CO2 laser 2 Nondestructive treatment: Excision

a. Margin for <2 cm and well-dened: 3 mm (85% clearance) or 4–5 mm (95%).

Depth is cu of fat.

b. Margin for large/poorly dened: 5 mm (80% clearance) or 13–15 mm (95%).

c. Mohs micrographic surgery (MMS) for high-risk lesions in cosmetically sensitive

areas.

d. Incompletely excised (5%) options: Observe, re-excise +/− frozen section, Mohs,

radiotherapy.

Radiotherapy

Cure rates similar to surgery. First-line or adjuvant for incompletely excised tumours. Contraindicated for recurrent tumours in previously irradiated areas. Usually reserved for elderly.

Advanced disease

Vismodegib if locally advanced (e.g. Gorlin’s syndrome). Electrochemotherapy if other treatment failed.

Follow-Up

Completely excised tumours: no follow-up. Incompletely excised tumours: observe (or treat) for recurrence.

Squamous Cell Carcinoma

Background

Second most common NMSC. Malignant neoplasm of keratinocytes. Arise de novo or from precursor lesion. Potential to metastasize. Metastatic risk is low (< 5%), but if there is metastasis, 25–40% 5-year survival.

Clinical Features

1 History: Lesion grows quickly (e.g. weeks/months), may ulcerate or bleed. 2 Examination: If well-dierentiated, has everted nodule and keratin core; if poorly dif-

ferentiated, may be ulcerated. Check lymph nodes.

Diagnosis

1 Punch or incisional biopsy. Key histologic features include keratin pearls. 2 Fine-needle aspiration for cytology, or radiology-guided core biopsy if there is an

enlarged lymph node.

3 Staging CT if there is deep invasion (e.g. bone/parotid) or evidence of spread.

Management

Principles

High-risk lesions have increased risk of local recurrence and metastasis. Factors include:

1 Macroscopic: Size >2 cm, site, recurrent lesions. Sites include chronic/radiotherapy

wounds, non-sun-exposed areas (e.g. sole of foot), sun-exposed areas (e.g. lip or ear). NB: Other sun-exposed areas are lower risk.

2 Microscopic: Histological dierentiation (e.g. poor is worst), Broder grade (e.g. 3/4 worst),

subtype (e.g. acantholytic/spindle/desmoplastic worst), depth (>4 mm or perineural invasion, etc.).

3 Systemic: Immunosuppression.

Key management: Decide if ‘high risk’, ‘xed’, or ‘regional/distant spread’. en AJCC stage.

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BENIGN AND MALIGNANT CONDITIONS OF THE SKIN

Surgical Treatment

1 Low-risk lesions (T1) have 4-mm margins, high-risk (T2 and above) have 6-mm mar-

gins minimum, ideally to fascia.

2 Consider MMS if high-risk or critical area. 3 Lymphadenectomy if there is regional disease.

Radiotherapy

SCC is radiosensitive. Radiotherapy is used as primary treatment or as an adjunct if there is incomplete surgical excision. However, radiotherapy does not give histology, is not curative if bone is involved, and over the long term can cause skin atrophy/telangiectasia, secondary cancer, or radionecrosis.

Melanoma

A malignant neoplasm of melanocytes. Accounts for 5% of skin cancers but 75% of skin cancer deaths.

Risk Factors

FPPARENTS mnemonic—Family history, Premalignant lesion (as above), Previous melanoma, Age (median 59), Race (Caucasian), Economic status, Nevus (>50), Fitzpatrick Types 1&2, Sunburn/sunbed.

Pathology

1 V60 0E gene codes for BRAF enzyme, if it is mutated, then there is BRAF mutation and

cell proliferation.

2 Ultraviolet radiation (UVA/B) damage to DNA.

Clinical Features

1 (Dermatoscopy) assessment—ABCD mnemonic: Asymmetry, Border irregularity,

Colour, Diameter >6 mm

2 Regional lymph nodes and systemic examination 3 Photography

Management

Initial

Excision biopsy with 2-mm margin to fat. Incisional (or punch) biopsies only performed if large lesion (e.g. lentigo) or subungual melanoma.

MDT

Discuss results with Specialist Skin multidisciplinary team (SSMDT). Biopsy helps give:

a. Subtypes: Supercial spreading melanoma (60%), nodular melanoma (30%), lentigo

maligna melanoma (7%), acral lentiginous melanoma (2%), desmoplastic melanoma (1%).

b. AJCC stage: Staging system splits melanoma into cutaneous (Table 76.4) and head and

neck mucosal, conjunctival, and uveal melanoma.

Investigation

1 Stages IIC and above need BRAF testing on primary or secondary lesion. 2 Stage IIC (if no sentinel lymph node biopsy [SLNBx]) or IIIB/C needs staging CT of

head & neck/chest/abdomen/pelvis.

3 Stage IV needs serum lactate dehydrogenase (LDH) +/− PET CT.

Nonsurgical

Psychological support, vitamin D, inform colleagues (e.g. transplant team) if patient is on immunosuppressants.

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BENIGN AND MALIGNANT CONDITIONS OF THE SKIN

Table 76.4 AJCC TNM staging for cutaneous melanoma

T: Primary tumour

Tx Thickness cannot be assessed T0 No evidence Tis Melanoma in situ T1a Breslow <0.8 mm thick without ulceration T1b <0.8 mm with ulceration

0.8–1 mm T2a 1.1–2 mm T2b 1.1–2 mm with ulceration T3a 2.1–4 mm T3b 2.1–4 mm with ulceration T4a >4 mm T4b >4 mm with ulceration

N: Regional lymph nodes

Nx Not assessed N0 No regional node metastasis N1a 1 occult node (i.e. SLNB) N1b 1 clinical node N1c No nodes, presence of in-transits/satellites/microsatellite N2a 2–3 occult nodes N2b 2–3 nodes, at least 1 clinical N2c 1 lymph node with presence of in-transit, satellite, or

microsatellites

N3a >4 occult nodes N3b >4 nodes, at least 1 clinical N3c >2 lymph node with presence of in-transit, satellite, or

microsatellites. Matted nodes

M: Distant metastasis

M0 No metastasis M1a Distant skin, soft tissue, or nonregional lymph nodes M1b Lung M1c All sites (not CNS) or raised LDH with any metastasis M1d CNS metastasis

Stage 5-year survival (%)

0 TisN0M0 — IA T1aN0M0, T1bNoMO 97 IB T2aN0M0 92 IIA T2bN0M0, T3aN0M0 81 IIB T3bN0M0, T4aN0M0 70 IIC T4bN0M0 53 IIIA T1a/b–T2a,N1/N2a,M0 78 IIIB T0N1b/cMo, T1a/b–T2aN1b/cN2bM0, T2b/

T3aN1a–N2bM0

IIIC T0N2b/cN3b/cM0, T1a–T3aN2c/N3abcM0, T3b/

T4a any N > 1M0, T4bN1a–cN2cM0

IIID T4bN3a/b/cM0 — IV Any T/N M1 15–20

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BENIGN AND MALIGNANT CONDITIONS OF THE SKIN

Table 76.5 WLE margins for melanoma

Thickness (mm) WLE (cm)

In situ 0.5 <1 1

1.01–2 1–2

2.01–4 2–3 >4 3

Local Surgery

1 Wide local excision (WLE; Table 76.5) reduces micrometastases (i.e. WLE for local

control).

2 MDT decision if there is to be MMS for indistinct margins (e.g. LM) or tumour in

critical areas (e.g. eyes).

Lymph Node Surgery (Stage III)

1 SLNBx for IB–IIC and for pT1b if lymphovascular invasion/mitotic rate > 2. SLNBx

is for staging/prognosis and guides adjuvant therapy but has no therapeutic/survival advantage. If positive SLNBx, follow up with examination +/− ultrasound of nodes +/− systemic treatment.

2 Indications for dissection (NB: Head and neck involve levels 1–5 +/− supercial

parotidectomy):

a. Post SLNBx:

i. If SLNBx shows features of risk of regional relapse (e.g. extracapsular spread

or >3 nodes involved)

ii. Dewar criteria

iii. In head & neck and there is concern later surgical rescue would be complex

iv. Failed rst-line systemic treatment and node-only recurrence

b. Palpable/imaged IIIB/C positive for melanoma following FNAC or image-guided

core/open biopsy (if FNAC negative/equivocal)

3 NB: ere is no evidence of survival benet for ‘elective’ lymph node dissection.

Metastatic Disease (Stage III or IV)

1 Options:

a. Immunotherapy (checkpoint inhibitors)—Pembrolizumab/nivolumab (anti-PDL1)

or ipilumab (CTLA4 inhibitor)

b. Targeted therapy if BRAF mutation—Vemurafenib/dabrafenib (BRAF inhibitor),

or trametinib (MEK inhibitor), or imatinib (targets C-KIT gene)

c. Interleukin-2

d. Chemotherapy (e.g. dacarbazine)

2 Further locoregional recurrence options: Systemic therapy, surgical excision if isolated

lesions, CO2 laser or electrocautery if multiple small lesions, radiotherapy for symptoms, electrochemotherapy if larger area.

Rare Skin Cancers

Merkel Cell Carcinoma

Aggressive and rare—has special AJCC TNM. Dermal neuroendocrine carcinoma. Associations include polyomavirus, previous radiation, B-cell lymphoma. Immunosuppression is a risk factor. Rapid, painless, enlarging, dome-shaped solid nodule on head and neck (50%). Lymph nodes may be involved at presentation (15%). Need tissue

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BENIGN AND MALIGNANT CONDITIONS OF THE SKIN

biopsy. Subsequently, staging CT. Discuss in MDT. Wide excision with 2- to 3-cm margins to fascia, as well as SLNBx and adjuvant radiotherapy to primary site +/− regional nodes.

Sebaceous Carcinoma

Aggressive and rare. From sebaceous glands. Risk factors include Muir-Torres syndrome. Firm yellowish nodule, especially near eyelids (75%). Obtain tissue diagnosis. Discussion in MDT. Requires wide excision with minimal 5-mm margins or Mohs (33% risk of recurrence). If orbit involved, exenteration.

Dermatobrosarcoma Protuberans

Most common skin sarcoma. Approximately 15% occur in head and neck. Incidence greatest in patients 20–40 years old. Intermediate malignancy, prone to local recurrence but not metastasis. Slow-growing, red/brown nodule xed to dermis. Obtain tissue biopsy. Discuss in MDT. Requires ~3-cm margins to fascia or Mohs. If unresectable or there are metastases, consider radiotherapy or chemotherapy (imatinib).