Which part of the brain is involved in the temporomandibular joint?

Brain Regions Involved in Temporomandibular Joint Function and Pain Processing

The temporomandibular joint is primarily controlled by the trigeminal nerve (CN V) for sensory and motor innervation, with central processing involving multiple cortical and subcortical regions including the inferior parietal cortex, precentral gyrus, amygdala, dorsal raphe nucleus, cerebellum, and pain-modulatory networks such as the default mode network, central executive network, and salience network 1, 2, 3.

Peripheral Neural Control

The TMJ receives direct innervation from the trigeminal nerve (CN V), specifically the mandibular division (V3), which provides:

• Motor innervation to the muscles of mastication (masseter, temporalis, medial and lateral pterygoids)
• Sensory innervation to the joint capsule, surrounding tissues, and facial regions 4, 5

The facial nerve (CN VII) also plays a role in TMJ surgery complications, with the temporal, buccal, and marginal mandibular branches at risk during surgical procedures, particularly TMJ replacement operations which account for 40% of facial nerve injuries in oral and maxillofacial surgery 6.

Cortical Processing Regions

Motor and Sensory Integration Areas

In healthy individuals observing jaw movements, sequential cortical activation occurs in:

1. Occipitotemporal region (MT/V5 area) - visual motion processing
2. Inferior parietal cortex (IPC) - sensorimotor integration
3. Anterior inferior-lateral precentral gyrus (PrCG) - motor planning and execution

Critical finding: TMD patients show marked deficit or attenuation of neuromagnetic responses in the PrCG and IPC during jaw movement observation, while MT/V5 activity remains normal. This indicates specific cortical dysfunction in visuomotor integration mechanisms 7.

Pain-Related Structural Changes

Patients with painful TMD demonstrate:

• Decreased cortical thickness in the left lateral occipital cortex

• Decreased fractal dimension (cortical complexity) in:

  • Left paracentral cortex
  • Right pars opercularis
  • Right rostral middle frontal cortex
  • Left lingual cortex
  • Right inferior temporal cortex 1

• Increased gray matter volume in:

  • Right putamen
  • Bilateral superior frontal gyrus
  • Right supplementary motor cortex
  • Bilateral postcentral gyrus
  • Right middle and inferior temporal gyri
  • Right temporal pole 2

Subcortical and Limbic Structures

Amygdala

The amygdala shows increased activation during persistent TMJ inflammation (10 days), particularly in:

• Basolateral nucleus
• Central nucleus

There is decreased expression of parvalbumin-positive (PV+) interneurons in the amygdala during chronic inflammation, with increased co-localization of PV+ and FosB/ΔFosB+ neurons, indicating altered inhibitory control and chronic neuronal activation 8.

Dorsal Raphe Nucleus

The dorsal raphe shows:

• Increased activation during persistent inflammatory phases
• Increased PV+ interneuron expression (opposite to amygdala pattern)
• Involvement in both sensory and affective dimensions of orofacial pain 8

Cerebellum

Beyond motor coordination, the cerebellum demonstrates:

• Altered spontaneous neural activity in TMD patients
• Strengthened functional connectivity with limbic structures
• Position-dependent connectivity changes based on mandibular position (centric occlusion vs. centric relation vs. stabilization splint) 9

Pain-Processing Networks

Triple Network Model

TMD patients show dysfunction across three interconnected networks 3:

1. Default Mode Network (DMN)

• Abnormal activation of attention-related regions
• Associated with pain rumination
• Cortical atrophy in emotion and pain regulation regions
• Altered functional connectivity

2. Central Executive Network (CEN)

• Decreased activity and metabolism in pain regulation regions
• Abnormal activation in regions associated with negative emotions

3. Salience Network (SN)

• Aberrant activation in pain perception regions
• Metabolic changes correlating with negative emotional states
• Abnormal activation patterns linked to anxiety and depression

Clinical Implications

Diagnostic Considerations

The brain regions involved explain why TMD patients commonly present with:

• Chronic pain beyond the joint itself
• Negative mood disorders (anxiety, depression)
• Attention and cognitive difficulties
• Altered pain perception and central sensitization 3, 10

Treatment Response Monitoring

Successful treatment correlates with:

• Return to normal activity in attention and emotion regulation regions
• Normalization of cortical activation patterns
• These changes can potentially be used to evaluate treatment efficacy 3

Important Caveats

• The cortical dysfunction in TMD is specific to jaw-related motor observation - no differences are found when TMD patients observe other movements (e.g., palm opening) 7
• Central nervous system changes may represent both cause and consequence of chronic TMD pain
• The relationship between peripheral joint pathology and central neuroplastic changes remains incompletely understood 3, 10
• Individual variation is substantial, and neuroimaging findings require confirmation in larger prospective studies before clinical application 9