The knee is a pretty badly-designed joint. Evolution doesn't move towards perfection, but function. 
As bipedal (two-legged) creatures who evolved from quadrupedal (four-legged) ones, quite a few compromises and fudges have been made. 

[The shoulder is another good example. it is a heavily-modified hip (i.e. ball-and-socket joint), but one where the bony shape and supporting ligaments have to allow for such a large range of motion that it relies on the surrounding muscles for nearly all of its support and integrity, as well as on the function of all the other joints surrounding it.  You can read more about the weird and wonderful world of the shoulder complex here.]
​
But anyway, the knee...

It is a hinge joint, the largest joint in the body, sandwiched in between the two longest bones in the human body, the femur (thigh bone) and tibia (shin bone). 
This is a fairly bad idea to start with, because long levers generate a lot of force. 
Worse, it's not a very simple hinge joint. 
If it were, and could only bend forwards and backwards, and we wouldn't be able to walk on broken or uneven ground. 
So we have the longest bones (/levers), generating a huge amount of force, going into the largest joint, which is also extremely complex.

Back when we put all of our weight through four ‘knees’ instead of two, this was less of an issue. 
​We also tend to weight-bear with our knees more or less unbent. This provides a lot more opportunity for trauma. Contrast this with other mammals such cats, dogs, horses, chipmunks, etc. etc. 

​​The bottom of the thigh bone is a bit like the cartoon version of a bone, with two knobbly bits (called condyles) at the bottom.  These then (theoretically) meet, or articulate, with the relatively flat top of the shin bone.

This works about as well as you would imagine. 

Evolution’s workaround here was to put these two sort of cups, called menisci, on the top of the flat bit of the shin bone (rather poetically called the tibial plateau).  These allow the knobbly condyles to sit a bit more firmly on the top of the tibia.  

Now, of course, we have another structure that takes a lot of force, and can get injured. 

Most sports fans (not to mention players) will have heard of a torn meniscus.  I tore mine when I was about fourteen, and still remember it as one of the most exquisitely painful experiences of my life. As you can see in the diagram above, when the menisci (the 'C-shaped' things around the outside) are in place they cover most of the top of the tibial plateau.

​But wait! There's more!  It's not all about the menisci.  In a flash of evolutionary genius, the other main way that the knee is stabilised is by four... ...elastic bands,
Well, not literally, but they might as well be. 
The rubber bands (known as ligaments by the medical types) are actually just thickenings of the capsule that surrounds the joint. 
Again, sports buffs will probably recognise the terms medial and lateral collateral ligaments.  These refer to the ligaments on the inside, and outside, of the knee, respectively. 
The anterior and posterior cruciate (or 'cross-like') ligaments go between the femur and tibia, and can be seen (along with the menisci) sandwiched in there on the left.
​

​So we have this large, unstable joint subject to huge forces, that we hold in biomechanically-compromised positions. 

Almost everyone has heard of ‘frozen shoulder’, but very few have a good idea of what it entails.  To be honest, even the medical profession understands what happens quite well, but not so much the why, even though it was first described in the eighteen hundreds [i], and affects about three to five percent of the population [ii] . 

You may remember that to allow the shoulder to do everything it needs to, you need the bony joint surfaces and soft tissue structures to permit a lot of movement.  This means that the capsule that surrounds the shoulder, or glenohumeral joint, is baggy, with lots of folds.  The idea is (or was) that adhesions, or sticky bits, between the folds stopped the arm from moving as far as it could/should.  However, the evidence for these capsular adhesions is a bit controversial, which is why we now ‘stick’ (Sorry! Couldn’t resist!) to the term “frozen shoulder.” 

The current thinking is that is not an ‘adhered’ joint capsule, but rather a contractured one (‘contracture’ is the [?permanent] shortening or hardening of a muscle or joint).  So rather than that nice baggy capsule with lots of loose folds that have stuck to each other, you have a sort of tightening, like shrink-wrap.  We still don’t know why that might happen, though!

Anyway, the long and short of it is that we do not really know what causes frozen shoulder syndrome (FSS). As with many conditions, FSS can occur on its own, or as a result of other issues.  The first is called primary or idiopathic frozen shoulder, whereas if it is associated with other diseases and conditions, it is called secondary frozen shoulder. 

Despite the lack of any particularly compelling evidence to link frozen shoulder with any one particular factor, several issues are thought to trigger FSS:

Trauma such as a rotator cuff tear (see previous blog!), broken arm or even surgery – it should be noted that is [obviously] more common after shoulder surgery, but not limited to such.

Metabolic/endocrine/hormonal such as thyroid disease, diabetes mellitus and other auto-immune disorders, where the body’s own immune system naively but enthusiastically attacks things wrongly identified as intruders [iv],[v],[vi],[vii],[viii]. With female sufferers (whom are affected more than men), onset is often around the same time as the menopause, implying a hormonal link [ix].

Neurological issues such as stroke and Parkinson’s disease can also trigger FSS.

Heart problems such as ischaemic heart disease (not getting enough blood to the heart) and hypertension (high blood pressure) have also been implicated.

Drugs, for instance some antibiotics and antiretrovirals (and other drugs, such as the grandiosely-named protease inhibitors, used to treat HIV). Some people also report developing FFS after immunisations, such as influenza or pneuomococcus.
Probably the biggest factor that we know about is inactivity. Most patients with FFS have undergone some period of shoulder immobilization, for one reason or another.  This may be one of the ways that surgery has an impact (you are normally asked to not move around too much immediately after an operation).  One study looked at patients undergoing neurosurgery who had immobilized shoulders for various periods, and found that the incidence of FFS was 5-9 times greater than in the general population[x].
 
So, the typical presentation for frozen shoulder would be someone in their fifties or sixties (peak age of onset being mid-fifties), more likely to be a woman than a man, and with a history of one or more of the above-listed factors, likely involving not moving one or both arms for a prolonged period. Interestingly, the non-dominant shoulder is slightly more likely to be affected.

The symptoms of frozen shoulder have traditionally been divided into three phases, and given the catchy monikers of freezing, frozen, and thawing.

Freezing (Stage 1) is characterised by gradual onset of diffuse (widespread, difficult-to-localise) shoulder pain. This stage can last from weeks up to nine months or so, but a year is not unheard-of.

Frozen (Stage 2) constitutes a gradual, progressive loss of shoulder range of movement.  You may find that it is not actually that painful in this stage, and the frustration comes more from not being able to bloody lift your arm than unremitting agony.  Unfortunately, guys, this stage can last anywhere from a few months to nearly two years (four to twenty months would be a quoted figure).

Thawing (Stage 3) consists of a phase of gradually (but not necessarily constantly) increasing range of movement.  This can also be a protracted stage, ranging from another few months (ok, around 4-5) to another couple of years (well, 26-odd months).
It is extremely rare to get frozen shoulder bilaterally (on both sides) at the same time (Thank goodness!), but around 6-17% of poor, limp-armed patients who have recently recovered from a bout of FFS will find an ominously-familiar ache in the other shoulder within five years, although recurrence in the same shoulder is unlikely[xi],[xii].

Next up I will discuss is the treatment options for Frozen Shoulder Syndrome (FSS)...

[i] Duplay S. De la periarthrite scapulo-humerale [On scapulo-humeral periarthritis]. Rev Pract D Trav De Med. 1896;53:226. French

[ii] Manske, R. & D. Prohaska, “Diagnosis and Management of of adhesive capsulitis” Curr Rev Musculoskelet Med. 2008 December; 1(3-4): 180–189

[iii] Codman, E.A. (1934) The Shoulder  Thomas Todd: Boston, MA

[iv] Bulgen, D.Y., Binder, A., Hazleman B.L. et al (1982) “Immunological studies in frozen shoulder” Journal of Rheumatology 9(6):893-8

[v] Bulgen, D.Y., Hazleman B.L., & Voak, D. (1976) “HLA-B27 and frozen shoulder” Lancet 1(7968):1042-4

[vi] Morén-Hybbinette I, Moritz U, Scherstén B (1987) “the clinical picture of the painful diabetic shoulder--natural history, social consequences and analysis of concomitant hand syndrome” Acta Med Scand. 1987;221(1):73.

[vii] Lequesne M, Dang N, Bensasson M, Mery C (1977) “Increased association of diabetes mellitus with capsulitis of the shoulder and shoulder-hand syndrome” Scand J Rheumatol. 1977;6(1):53

[viii] Huang YP, Fann CY, Chiu YH, Yen MF, Chen LS, Chen HH, Pan SL (2013) “Association of diabetes mellitus with the risk of developing adhesive capsulitis of the shoulder: a longitudinal population-based followup study” Arthritis Care Res (Hoboken). 2013 Jul;65(7):1197-202.

[ix] Ewald, A. (2011) "Adhesive capsulitis: A review" American family physician 83(4):417–422

[x] Bruckner FE; Nye CJ (1981) “A prospective study of adhesive capsulitis of the shoulder ("frozen shoulder') in a high risk population” Q J Med.  1981; 50(198):191-204

[xi] Rizk TE, Pinals RS. “Frozen shoulder” Semin Arthritis Rheum. 1982;11:440–452.

[xii] Guyver PM, Bruce DJ, Rees JL “Frozen shoulder - A stiff problem that requires a flexible approach” Maturitas. 2014 May; 78(1):11-6.

Picking up where we left off last time.....
 
We were discussing the intricacies of the shoulder complex, and its relationship with surround body structures and areas.  We noted that the shoulder is extremely mobile, with very little in the way of bony congruency (stability from the shape of the joint(s), and hence relying on the supporting musculature.

A particularly important group of these is known as the rotator cuff, so called because they form a cuff around the top of the arm bone and are (surprise surprise!) responsible for arm rotation.  54% of asymptomatic (i.e. not having pain or problems) patients aged 60 years or over were found to have partial or complete tears of the rotator cuff on MRI (a type of imaging), which should give you some idea of how hard those poor little fellows work over the course of our lives.

So why does the rotator cuff have to work so hard?
As previously mentioned, the shoulder is an incredibly mobile [series of] joint[s], and allows incredible mobility, but at the expense of stability.

There is a fibrous capsule surrounding the shoulder joint proper (the glenohumeral joint), as there is around many/most of the joints in the body. In the shoulder, this fibrous layer is both thin and loose, allowing a wide range of movement.  The tendons of the rotator cuff blend with and reinforce this fibrous layer of the joint capsule, helping to protect and stabilize the joint.
 
Although they all have separate functions (some turn the arm out and the shoulder, others inwards etc.), the rotator cuff muscles work as a group to hold the head of the humerus (top of the arm bone) in the glenoid fossa (remember I described the shoulder as not so much of a ball-and-socket, but as a ball-and-tiny-saucer?). The glenoid fossa is the technical term for that little saucer-shaped depression) during arm movements.  They also passively support the dependent (hanging) humerus while sitting or standing, especially supraspinatus. The arm would dislocate downwards out of this socket were it not for the rotator cuff (and the angle of the fossa).  They also work with the bigger deltoid muscle to lift the arms out to the side.

In short, the rotator cuff helps us to support the shoulder and control fine movements that then enable us to use the wonder of evolution, the hand, and lets your move your arms around over your head without everything smashing together.

Common injuries of the rotator cuff
Rotator cuff overuse issues start early in life, with oedema (swelling) and haemorrhage (bleeding) of the tendon and bursa.  This can start before the age of twenty five.

Stage II involves fibrosis and tendinitis, that is, the thickening and scarring of connective tissue (a general term that includes tendons, ligaments, cartilage, bone, and even fatty tissue and blood, but for these purposes refers to the tendons of the muscles) and inflammation/irritation and degeneration of the tendons.  This broadly speaking takes place from the ages of around 25-40 years of age.

Stage III involves tearing of the rotator cuff, which can be either partial or full-thickness tears, and typically takes place over the age of 40.

Additionally, rotator cuff pathology is often bilateral (both sides), even when one side only is symptomatic (painful), and those with one painful side have been shown to be at risk of developing pain and tear progression on the other side (see refs at bottom of page). This is possibly related to compensatory overuse of the non-painful side.

It is also possible to have an acute or sudden-onset tear, often caused by a fall onto an outstretched arm, or trying to lift/catch something unexpectedly heavy.  These may occur with or without the above-mentioned changes over time.

Bursitis is when a small fluid-filled sac that is designed to cushion from shock/friction itself gets irritated or infected.  The most common bursitis in the shoulder of the subacromial bursa.

Impingement syndrome happens when outer end of the shoulderblade, called the acromion, contacts or impinges on the tendon, bursa, or both.

Primary impingement is due to structural issues (i.e. how we are built).  Some of us have smaller sub-acromial spaces than others. Osteoarthritis (wear and tear) can make this worse due to little bony spurs called osteophytes that further reduce this space.

Secondary impingement is normally a result of dynamic instability (i.e. how we use our shoulders). If the rotator cuff muscles are weak, they do not do their job well; so are unable to prevent the head of the humerus from riding up into the sub-acromial space as we lift our arm.  This also leads to pinching of the tendon and/or bursa.
Of course, inflamed/swollen tendons and bursae also take up more room, further decreasing the potential sub-acromial space, so these problems can co-exist and reinforce each other.

An Honourable Mention… goes to bicipital tendinopathy, which is inflammation/irritation of the long head of biceps tendon or its sheath. 

It is rarely seen in isolation, and normally co-exists with rotator cuff pathology/impingment or other shoulder issues.  Like the above, it is normally caused by overuse/degenration, shoulder instability, tendon impingment or trauma.

Stay tuned to our next blog installment on the shoulder, treatment..

References

[i]  Mall NA, Kim HM, Keener JD, et al. Symptomatic progression of asymptomatic rotator cuff tears: a prospective study of clinical and sonographic variables. The Journal of bone and joint surgery American volume. 2010;92(16):2623–33

[ii]  Moosmayer S, Tariq R, Stiris M, Smith HJ. The natural history of asymptomatic rotator cuff tears: a three-year follow-up of fifty cases. The Journal of bone and joint surgery American volume. 2013;95(14):1249–55