Primary Sites of Oropharyngeal Tumors[1,
7]
1) Base of Tongue (BOT)
(Fig. 8, Fig. 9, Fig. 10, Fig. 11, Fig. 12, Fig. 13, Fig. 14)
Tumours of the BOT are insidious,
often clinically occult and therefore present in advanced stages.
Unilateral involvement of the BOT is common,
crossing the midline only when the tumour becomes too large.
MRI is the modality of choice in assessing the extent of the lesion.
Axial images are superior in assessing the size,
midline spread and the involvement of the soft palate and tonsillar region.
Coronal images are useful in evaluating the floor of mouth,
while the sagittal images provide information on the extent of pharyngeal infiltration.
Involvement of deep intrinsic muscles of the tongue is best assessed on MRI
2) Tonsil
(Fig. 15, Fig. 16, Fig. 17, Fig. 18, Fig. 19)
The tonsillar region is the most common site of oropharyngeal SCC development[9].
Tumours can originate from the tonsils,
the tonsillar fossa,
the anterior tonsillar pillars or the posterior tonsillar pillars with the anterior tonsillar pillars being the most common sites of primary lesions.
Lesions are often exophytic or ulcerative in nature.
SCC within the tonsillar fossa are mostly clinically occult and may present initially with cervical lymphadenopathy.
Lesions often involve either the anterior or the posterior tonsillar pillar and therefore acquire the spread patterns of the lesions located in those regions.
Isolated tumours of the posterior tonsillar pillars are rare and lesions are usually smaller than those found in other tonsillar regions.
3) Soft palate/Uvula
(Fig. 20, Fig. 21)
Tumours of the soft palate tend to be superficial and well differentiated.
They are mostly diagnosed in the earlier stages and have better prognosis than other SCC of the oropharynx.
The oral aspect of the soft palate is the most common location of SCC occurrence whereas the nasopharyngeal aspect is often speared even when the lesion is large.
4) Posterior pharyngeal wall
(Fig. 22)
SCC originating from the posterior pharyngeal wall are rare and carry poor prognosis.
Tumours commonly presents as exophytic mucosal masses extending to the nasopharynx or the hypopharynx.
Miscellaneous malignant tumors
SCC are the most common malignant tumors found in the oropharynx.
Other rare malignant tumors include minor salivary gland carcinomas (Fig. 23, Fig. 24),
lymphomas and lymphoepitheliomas.
Minor salivary gland carcinomas have the highest frequency of occurrence in the posterior hard palate and the soft palate[7].
Non-Hodgkin’s lymphoma presents as extranodal lymphatic disease due to the abundance of lymphoid tissues in the oral pharynx,
they present as large,
homogenous lesions on imaging studies.
Lymphatic Spread
SCC of the oropharynx predominantly drain into cervical lymph nodes level II,
level III (American Joint Committee on Cancer (AJCC)) (Fig. 25)and also the retropharyngeal nodes which are not covered by the standard nodal system.
Level II nodes are located between the base of skull and the lower body of the hyoid bone; posterior to the back of the submandibular gland and anterior to the posterior border of the sternocleidomastoid (SCM) muscle.
Level III nodes are between the lower body of the hyoid and the lower cricoid arch,
lateral to the medial margin of the common carotid artery and anterior to the posterior border of the SCM.
The retropharyngeal nodes which are within 2cm of skull base and medial to the internal carotid arteries are divided into the medial and lateral groups; the medial group is found in the suprahyoid retropharyngeal space,
the lateral group is located between the carotid artery and the longus colli muscles.
Lymphatic involvement is the single most important prognostic factor.
Of patients with oropharyngeal SCC,
approximately 65% will have cervical lymphadenopathy.
In particular,
SCC of the BOT has the highest potential of lymph node involvement,
followed by SCC of the tonsillar fossa.
Bilateral nodal involvement is more prevalent with tumours of the posterior pharyngeal wall,
soft palate and the base of tongue as extension beyond the midline is common.
The cardinal features of malignancy are enlargement,
heterogeneity and necrosis.
With regards to the size criteria,
malignancy is indicated if the maximum longitudinal diameter is greater than 15mm for jugulodigastric nodes (part of leveII),
greater than 8mm for retropharyngeal nodes or greater than 10mm for any other nodes.
However,
if more than 3 nodes of greater than 8mm are found in the same lymphatic drainage area,
nodal metastasis is also likely[1].
CT is the primary imaging modality in detecting nodal involvement of oropharyngeal SCC.
Other than the size criterion,
other crucial findings of malignancy include the loss of ovoid shape,
heterogeneous enhancement with necrotic centres and extracapsular spread.
HPV+ve SCC may also present with cystic adenopathy which may be mistaken for benign lesions. Contralateral or bilateral involvement of cervical nodes are often associated with large tumours crossing the midline and shows strong correlation with a worse prognosis[10,
11],
therefore requires more aggressive treatment.
In the presence of streak artefacts from dental fillings or the involvement of the retropharyngeal nodes are suspects,
MR imaging becomes the modality of choice.
Extracapsular spread increases the rate of local recurrence by 3.5times[1] and is best demonstrated using MRI.
Features of extracapsular spread include poorly defined nodal margins,
irregular rimlike enhancement and increased soft tissue intensity surrounding the nodes.
Neurovascular Invasion
Invasion of local neurovascular structures are highly suggestive of distal metastasis.
Perineural spread is rare in the setting of oropharyngeal SCC.
Deep invasion of the carotid sheath leads to the encasement of the carotid artery which is best demonstrated on MRI.
If encasement of vasculature is present,
the tumour is deemed inoperable.
TNM Staging
The TNM staging process based on the AJCC is best used to describe,
oropharyngeal SCC whilst also assists in predicting the prognosis and constructing treatment plans. (Table 1)
Primary Tumors - Pathways of Spread[1,
8,
9,
12]
- Base of Tongue (Fig. 26):
-
- Tumors usually spread along the palatoglossus muscle to involve the anterior tonsillar pillar; or spread anteriorly into the body of the tongue and the floor of the mouth.
- Tongue base tumor can cross the glosso-tonsillar sulcus and involve the tonsillar fossa
- Tumours may also invade inferiorly,
affecting the vallecula and the pyriform sinus and into the pre-epiglottic space.
- Inferolateal spread into the deep soft tissues of the neck may eventually lead to the involvement of the styloid musculature and the internal carotid artery.
- Tonsils (Fig. 27):
-
- Tumors of the anterior tonsillar pillars commonly invade the palatoglossus muscle superiorly to involve the lateral aspect of the soft palate.
- Tonsilllar primaries commonly cross the glosso-tonsillar sulcus and involve the tongue base
- Other sites of spread include retromolar trigone and the buccal mucosa.
In advanced cases,
lesions may involve the parapharyngeal space,
the mandible and/or spread along the pharyngeal wall to the naso/hypo-pharynx. In advanced stages,
spread to the skull base along the tensor and levator veli palatini muscles may be seen.
- Lesions found on the posterior tonsillar pillar tend to spread along the palatopharyngeus muscle superiorly to involve the soft palate,
inferiorly to involve the thyroid cartilage,
the middle pharyngeal constrictors and the pharyngoepiglottic fold.
- Soft Palate (Fig. 28):
-
- Although tumours can extend in any direction,
anterior spread is the most common and therefore the hard palate and the tonsillar regions are often the first structures to be affected.
- Deep invasion of the parapharyngeal space along the tensor veli palatini and levator veli palatini muscles laterally is rare and is seen in advanced stages,
where they may be associated with the involvement of the external carotid artery and skull base.
- Neural spread along the palatine branch of the maxillary nerve,
the greater and lesser palatine nerves to the skull base can occur which may lead to the involvement of the cavernous sinus.
- Posterior Pharyngeal Wall (Fig. 29):
-
- SCC of the posterior pharyngeal wall are commonly found to spread into the retropharyngeal space and infiltrate the prevertebral fascia.
Involvement of the prevertebral space and the paravertebral muscles precludes surgery.
- Lesions can also spread superiorly into the nasopharynx or inferiorly to involve the pyriform sinus and the hypopharyngeal wall.
- Most lesions cross the midline and therefore bilateral cervical lymph node involvement is common.
Difference between HPV+ and HPV- SCC of the oropharynx
HPV+ve SCCs (Fig. 30)tends to present with smaller,
exophytic lesions with well-defined borders,
they are associated with bulky cervical nodal involvement of cystic appearance on CT.
HPV+ve SCCs are more likely to arise from the BOT and the tonsils than their HPV-ve counterparts[13].
On imaging,
HPV-ve SCCs (Fig. 31) display ill-defined borders,
invasion of adjacent muscles is also common.
Compared to HPV+ve SCCs of the oropharynx,
HPV-ve SCCs are diagnosed at later stages and are also associated with a worse prognosis[5,
6].
Discussion and Management
Although head and neck cancers display a decreasing trend globally,
the incidence of oropharyngeal cancers is rising.
This is particularly due to the clinically occult nature of oropharyngeal tumours and the increase in the incidence of HPV positive oropharyngeal SCC.
Currently,
the diagnosis and staging relies on using imaging studies,
predominantly CT scans and MR Imaging.
As SCC of each subsite displays their unique spread patterns,
information regarding the tumour and the extent of spread can be assess with great accuracy using the aforementioned modalities.
The management of oropharyngeal SCC depends on the stages of the presenting tumours.
Smaller lesions (T1 or T2) are usually treated with single modality therapy (either radiotherapy (Fig. 32,
Fig. 33) or surgery).
However structures such as the soft palate or the uvula have significant role in palatal function therefore are often managed with radiotherapy[8].
Large tumours may be treated surgically with adjuvant radiotherapy.
In the case of inoperable tumours and those with relative contraindications to surgery such as bilateral involvement of the base of tongue,
extension of the tumour to the larynx,
combined chemotherapy and radiotherapy is the treatment of choice[8].
In the presence of nodal involvement,
neck dissection is usually indicated with curative intent.
Due to the predictable pattern of spread of oropharyngeal SCC,
selective dissection of the lateral neck (levels II – IV) will most often suffice.
The area of which is marked by the medial border of the sternothyroid and the posterior border of the sternocleidomastoid,
extending from the skull base to the clavicle.
The spinal accessory nerve,
internal jugular vein and the sternocleidomastoid muscle are spared in this procedure.
In the presence of extensive nodal disease,
i.e.
presence of N3 nodes,
clinically evident nodes,
involvement of neurovascular or musculoskeletal structures,
extranodal spread or recurrence of nodal disease,
a radical neck dissection is indicated.
Radical neck dissection involves the removal of all ipsilateral nodes from level I through to V and also the spinal accessory nerve,
the internal jugular vein and the sternoceidomastoid muscle.
A modified radical dissection can also be performed when one or more of the aforementioned non-lymphatic structures can be preserved.
The name(s) of which should be included in the procedural detail.
In case of more advanced disease,
the radical neck dissection may need to include structures outside the scope described above in order to achieve negative margins.
The procedure therefore will be termed extended neck dissection and the procedural details should include the structures resected e.g.
the retropharyngeal nodes,
the hypoglossal nerve or the prevertebral musculature.