When vitamin D and calcium meet up, they bond together in the blood vessels first, then initiate the process of calcification when there is enough level of calcium in the blood. Therefore, bones begin to construct and repair themselves through calcification in the body's skeletal system (Paschalis et al., 2017).

Primary healing occurs when the internal fixation is rigid. Fixation provides stability for reconstructing the linkage between healthy and fractured bones (Gu, 2019, para. 2).

Secondary healing occurs when the fixation is fragile and will need to undergo four phases to fully recover: inflammatory response, soft callus formation, hard callus formation, and bone remodelling (Gu, 2019, para. 3). 

Oestrogen and calcium play a prominent role in constructing and maintaining the stability of bones. If the body is lacking these contributors, this will cause a diminished amount of bone density, which will increase the possibility of bone loss and fractures (Mayo Clinic, 2019, Hormone Levels & Dietary Factors section).

Additionally, if the body has too much thyroid hormone, this can cause bone loss due to the increased excretion of calcium and phosphorous via urine and stool as well as causing the rise of calcium levels in blood up to twenty-five per cent (Mayo Clinic, 2019; MedicineNet, 2018).

T4 and T3 are the regulators that control the functioning rate of our body cells and it’s important to have a balanced amount of them to allow our body to function in harmony (British Thyroid Foundation, 2019). 

If there are too many of these hormones, our body will work faster than normal health conditions such as having a faster heart rate and increased metabolic activities throughout the body system (British Thyroid Foundation, 2019). 

If there is a lesser amount of T4 and T3 in the body, the overall metabolic activities within the body will slow down and will cause a slower heart rate and a decrease in bowel movements, which will directly cause constipation to the body (British Thyroid Foundation, 2019).

During the meet-up, the acetylcholine quickly befriends its new mate, Botox, and they start to enjoy dancing and having fun together. In the meantime, acetylcholine forgets its important job in contracting muscles by interacting with its old pal, “SNARE protein” or “Snap Receptor protein” (Nigam & Nigam, 2010). 

Therefore, the occupied acetylcholine temporarily leaves SNARE protein for vacation, which then causes paralysis in the injected area (Nigam & Nigam, 2010).

T-tubules are home to dihydropyridine receptors which interact with the sarcoplasmic reticulum via the ryanodine receptor (Cogné et al., 2017). Once the reaction between these two receptors initiates, it signals the calcium ions (that are stored in the sarcoplasmic reticulum) to leave the cell into the cytoplasm (Cogné et al., 2017). Calcium ions then enable the cross-bridge muscle contraction cycle (Cogné et al., 2017).

These electrolytes are essential for the nerves to properly function, and nerves are in charge of signalling the muscle cells to contract and relax by triggering the muscle’s action potential to let sodium and potassium move in and out of the muscle cells (Koonce, 2018).

For example, when the muscle is at the resting state, sodium has a higher concentration outside of the muscle cells than the ones inside the cells, and potassium has a lower concentration outside the muscle cells than the ones inside the cells (Koonce, 2018).

As the nerve tells the muscle fibre to contract, sodium swiftly moves into the muscle cells, and potassium flows out of the muscle cells to give space for the sodium to stay inside the cells (Koonce, 2018).

When the muscle fibre relaxes, sodium trickles out of the cells, and potassium re-enters the muscle cells (Koonce, 2018).

Therefore, this is why I feel like sodium and potassium are like the fun-loving kids who love playing slides in the park, and they always wait for their turn in a queue to play the slides safely.

Muscle tone helps generate reflexes for the body and also assists in maintaining the proper function of the organ systems within the body (Libretexts, 2020).

On the other hand, muscle spindles are the sensory units that regulate the muscle tone within the body, and muscle spindles operate through a feedback loop by triggering the associated muscles’ motor neurons to transmit nerve impulses (Libretexts, 2020).

Muscle spindles also contain sensory neurons so they can transmit information about the stretching degree of a particular muscle by stretching their sensory neurons to send the nerve impulses to the cerebral cortex as well as generating a rapid reflex through sending nerve impulses to the spinal cord when they stretch their sensory neurons (Libretexts, 2020).

When the muscle tone is decreased and the muscle stretches the spindles, this will lead to muscle contraction and the muscle spindle will no longer stretch its sensory neurons to send nerve impulses (Libretexts, 2020).

Although Botox’s common usage is to bring facial muscles that cause wrinkles in the forehead and muscles around the eyes into transient relaxation, Botox can also be used to treat conditions such as cervical dystonia (neck spasms), lazy eye, muscle contractures (loss of muscle’s elasticity), hyperhidrosis (excessive sweating), chronic migraine, bladder dysfunction, and eye-twitching via intramuscular injection (Mayo Clinic, 2021).

In the central nervous system, oligodendrocytes are the myelinating cells that are in charge of generating myelin in the glial cells and are created by oligodendrocyte progenitor cells (Multiple Sclerosis Trust, 2018; Kuhn et al., 2019).

Myelin is an extended membrane that wraps up the axon like a hot dog with a bun which helps the axon speed up the delivery of nerve impulses to synapses and dendrites to complete a series of neural transmissions in the body’s nervous system, as well as protecting the axons from toxins and disturbing factors that may cause potential damage to the nerves (Kuhn et al., 2019; Mayo Clinic, 2020).

Once the nerves have become demyelinated, the nerve impulse transmission to the central nervous system will become delayed and blocked if severe, and this will also cause a range of symptoms such as multiple sclerosis, schizophrenia, and Alzheimer’s disease, etc (Multiple Sclerosis Trust, 2018; Kuhn et al., 2019).

Speaking of minimal display of regeneration in the central nervous system, especially in the lesions of multiple sclerosis, the process of proliferation and maturation of oligodendrocytes are usually impaired and even dysfunctional and are lesser in density than the ones in the undamaged nerves (Podbielska et al., 2013). This is most likely the main reason why the remyelination process (restoring myelin sheath on axon) is poorly conducted exclusively in the late stage of multiple sclerosis within the body’s nervous system (Podbielska et al., 2013).

Saltatory conduction occurs within the myelinated axons and its conduction process is much faster than continuous conduction due to the presence of myelinated sheaths and their shorter travelling length (Gibson, 2020). 

During the saltatory conduction, nerve impulses mobilise by leaping from one unmyelinated gap to another through the myelinated axons, which allows the nerve impulses to travel quicker to their destination as if at the speed of lightning (Gibson, 2020).

Similarity-wise, they both require a certain amount of electron particles to reach a threshold level for the nerve impulse conduction to happen. After reaching the threshold level, the ions move across the axon by altering its resting membrane to the action potential state then travel through the voltage-gated ion channels to deliver the nerve impulse (Gibson, 2020).

In the somatosensory pathway, primary neurons assist in detecting the exterior stimulus such as senses of touch and temperature. They also assist in sending these nerve signals to the secondary neurons for further transmission to the brain (Libretexts, 2020). 

Secondary neurons are the relay stations for the nerve impulses to continue transmitting to the third neurons by crossing their axons to the opposite side of the spine to deliver them up to the brain (Libretexts, 2020).

As the nerve signals reach their destination in the cerebellum, of where the third neurons are, the neurons here will be in charge of forming a cortical homunculus that seamlessly initiates the body’s movements that correspond to the signals’ intents and sensory perception from the outside world (Libretexts, 2020). 

The dorsal column-medial lemniscal pathway (assists in receiving the sensations of fine touch and facilitating the joint positions in the body) and the spinothalamic cortical pathway (assists in receiving the sensations of pain and temperature) are two of the pathways within the primary somatosensory cortex and multiple sclerosis can cause impairment to these pathways (Scherder et al., 2018).

The loss of vibrational sensation and proprioception are possibly caused by the dysfunction in the dorsal column medial lemniscal pathway and it also correlates to the loss of sensation that occurs in hypoesthesia (Scherder et al., 2018).

The inhibition in processing nociceptive (pain receiving) information when the neural signals go through the unmyelinated C-fibres via beta fibres is the main cause that makes this pathway malfunction and these symptoms all happen in the cortical and spinal level (Scherder et al., 2018).

Therefore, this is the reason why chronic pain in joint positions and the loss of all forms of sensation are so common in individuals with multiple sclerosis due to the demyelination in the somatosensory pathways.