1.) Pain around the anterior aspect of the knee, which increases by the posture of prolonged knee bending or by going upstairs/downstairs.
2.) With instability, you get a feeling of giving way.

In properly selected patients the side effects are uncommon. However, some patients may develop urinary retention if the tape is too tight and need a release operation. Patients may also continue to have milder degrees of incontinence till fibrosis sets in or because of development of urgency. Both these can be treated with non operative methods. The success rates of above-mentioned procedures vary from 75% to 90%.

After assessment of the degree and type of stress incontinence, a stepwise plan can be made to treat an individual patient.
A.) Lifestyle interventions: These include weight reduction, dietary/fluid modification e.g caffeine intake.

B.) Supervised pelvic muscle training and biofeedback to improve muscle tone and inhibit unwanted bladder contractions.

C.) Drug treatment for UTI, antimuscarinics for overactive bladder and duloxitene for milder degrees of incontinence.

D.) Estrogen supplementation preferably as local treatment as per gynaecologist’s advice.

This initial treatment is tried for 8-12 weeks and can improve or cure a number of patients, particularly those with milder intermittent incontinence. Severe cases and those not responding to conservative treatment are offered surgical treatment. A number of surgical treatments are available which are minimally invasive. The most popular are :

a.) Retropubic suspension – procedures are used when urethral descent is the main defect, e.g. MMK, Burch colposuspension, Raz, etc.

b.) Sling procedures – popularized by Mcguire which involve placement of pubovaginal slings of fascia or synthetic materials and can be used for both types of defects.

c.) Mid urethral slings – these essentially increase urethral support and are useful even in cases of prolapse. They are tension free vaginal tapes(TVT) and the relatively safer TVT-O (that passes through obturator foramen on either side). They are best used in previously unoperated patients.

It is important to treat significant genitourinary prolapse at the time of doing sling surgery to prevent urinary obstruction.

d.) Injection of periurethral bulking agents is a good option in sphincteric type of defect but may not be permanent.

e.) An artificial urinary sphincter is another useful but very expensive device in sphincter deficient patients.

A proper history of incontinence episodes and past obstetric history and a detailed examination is enough to clinch the diagnosis. It is important to note the degree of genitourinary prolapse, document urethral descent by Q-tip test, ascertain tone of pelvic muscles and prove incontinence by Bonney Marshall test. It is therefore important to do a pelvic exam on full bladder.

In patients with mixed incontinence, it becomes mandatory to perform a urodynamic assessment to rule out overactive bladder before considering surgery. Urine analysis and urine culture should always precede specialized tests for other causes of urgency. Imaging studies alone give little information but can be of great help when combined with urodynamics as they tell the exact pathophysiology of stress incontinence.

Stress incontinence is commonly seen in middle-aged females and accounts for most cases of incontinence. It is multifactorial and in a significant percentage of cases is mixed, i.e. coexists with urgency or urge incontinence. Main contributing causes to stress incontinence are-lax pelvic muscles due to difficult or multiple childbirths, prolapse of uterus, postmenopausal status, poor urethral support and poor urethral sphincter function.

There are thus two main types of defects in a female with stress urinary incontinence :

1.) Genuine stress incontinence with descent of urethra and

2.) Intrinsic sphincter deficiency.
Most cases have a variable combination of these defects.

Incontinence is broadly of two types :

1.)Urge incontinence – associated with an uncontrollable desire to void.

2.)Stress incontinence– associated with increased intraabdominal pressure.

Involuntary loss of urine that is social and/or hygienic problem is called incontinence.

Depending on severity, premature ejaculation symptoms can be significantly reduced. In mundane cases, treatments are focused on gradually training and improving mental habituation to sex and physical development of stimulation control. In clinical cases, various medications are being tested to help slow down the speed of the arousal response.


Most sex therapists and sex educators prescribe a series of exercises to enable the man to gain ejaculatory control. These are considered the first line of treatment and are usually recommended to be tried before other methods.

One of the most common exercises is the “Start-Stop” technique in which during sex when he feels that he is getting too close to orgasm, he stops and does not move, to avoid more stimulation. He may withdraw his penis, or stay inside and request that the partner also not move. He waits seconds or minutes until his arousal lessens, and then resumes sex. He may stop and then re-start as many times as necessary.

Another technique is the “Squeeze Technique”, in which during sex(or masturbation if he wants to practice it) when he feels the urge to ejaculate, he would withdraw his penis and squeeze at the tip of the shaft below the glans of his penis near the frenulum of his penis, until the feeling subsides. To be more specific, the proper hand position for this technique is for him to place his thumb on frenulum, and his index and middle fingers above and below the coronal ridge(which is on the other side of the head of his penis), and then squeeze his penis from to back. He may consult a sex therapist for more directions to this technique.

The male’s partner plays an essential role in enabling him to overcome premature ejaculation. Without understanding and emotional support, the male is unlikely to obtain the level of relaxation required for sexual satisfaction. Both the male and his partner should communicate their feelings openly and with sensitivity. The partner may also be integrated into the exercises to keep her involved. She can learn to deliver the squeeze technique, and she can encourage the stop-start technique. Both partners should also aware of the sexual positions that make the male most likely to ejaculate quickly. They should avoid those positions if they want to prolong sex. Some men ejaculate quickly in any position, however, so the other methods would be more effective.

In cases where the chief concern is reaching simultaneous orgasm, it is also possible to simply work around the premature ejaculation problem by changing positions frequently(which studies have shown delays male orgasm by a factor of 2-3), using lubrication to reduce friction(friction stimulates the male but it is not as important in female orgasm), or switching to cunnilingus for awhile when close to ejaculation, and then switching back when ejaculation is no longer imminent.


SSRI antidepressants have been shown to delay ejaculation in men treated for different psychiatry disorders. SSRIs are considered the most effective treatment currently available for PE. These include paroxetine, fluoxetine, sertraline and more. The use of these drugs, that require chronic therapy, is limited by the neuropsychiatric side effects. New SSRI drugs specifically targeted to treat premature ejaculation(e.g. dapoxetine) can be taken on an ‘as needed’ basis have recently shown positive results in large phase III studies. Nevertheless, dapoxetine is not yet approved by any regulatory authority around the world. There is speculation that some of the associated effects are caused by lowered libido and blood pressure as well as lowered anxiety levels. Other pharmaceutical products known to delay male orgasm are opioids, cocaine, and diphenhydramine.

Local anesthetic creams(like lidocaine, prilocaine, and combinations) have shown to be effective in clinical trials and are being used for the treatment of PE. Their use is limited by their own anesthetic effect, that reduces sensation on the penis and vagina.

Psychological factors commonly contribute to premature ejaculation. While men sometimes underestimate the relationship between sexual performance and emotional well-being, premature ejaculation can be caused by temporary depression, stress over financial matters, unrealistic expectations about performance, a history of sexual repression, or an overall lack of confidence.

Interpersonal dynamics strongly contribute to sexual function, and premature ejaculation can be caused by a lack of communication between partners, hurt feelings, or unresolved conflicts that interfere with the ability to achieve emotional intimacy.

Neurological premature ejaculation can also lead to other forms of sexual dysfunction, or intensify the existing problem, by creating performance anxiety. In a less pathological context, premature ejaculation could also be simply caused by extreme arousal.

The neurotransmitor serotonin(5HT) has a central role in modulating ejaculation. Several animal studies have demonstrated its inhibitory effect on ejaculation modulated through the PGI system in the brain. Therefore, it is perceived that low level of serotonin in the synaptic cleft in these specific areas in the brain could cause premature ejaculation. This theory is further supported by the proven effectiveness of SSRIs, which increase serotonin level in the synapse in treating PE.

Sympathetic motor neurons control the emission phase of ejaculation reflex and expulsion phase is executed by somatic and autonomic motor neurons. These motor neurons are located in the thoracolumbar and lumbosacral spinal cord and are activated in a coordinated manner when sufficient sensory input to reach the ejaculatory threshold has entered the central nervous system.
Several areas in the brain, and especially the nucleus paragigantocellularis, have been identified to be involved in ejaculatory control.

Scientists have long suspected a genetic link to certain forms of premature ejaculation. In one study, ninety-one percent of men who suffered from lifelong premature ejaculation also had a first-relative with lifelong premature ejaculation.

Other researchers have noted that men who suffer from premature ejaculation have a faster neurological response in the pelvic muscles. Simple exercises commonly suggested by sex therapists can significantly improve ejaculatory control for men with premature ejaculation caused by neurological factors. Often, these men may benefit from anti-anxiety medication or selective serotonin reuptake inhibitors(SSRIs), such as sertraline or paroxetine, as these slow down ejaculation times. Some men prefer using anaesthetic creams, however, these creams may also deaden sensations in the man’s partner, and are not generally recommended by sex therapists.

Most men experience premature ejaculation at least once in their lives. Often adolescents and young men experience premature ejaculation during their first sexual encounters, but eventually, learn ejaculatory control.

Because there is great variability in both how long it takes men to ejaculate and how long both partners want sex to last, researchers have begun to form a quantitative definition of premature ejaculation. Current evidence supports an average intravaginal ejaculation latency time(IELT) of six and a half minutes in 18-30-year-olds.

If the disorder is defined as an IELT percentile below 2.5, then premature ejaculation could be suggested by an IELT of less than about one and a half minutes.

Nevertheless, it is well accepted that men with IELT below 1.5 minutes could be “happy” with their performance and do not report a lack of control and therefore does not suffer from PE.

On the other hand, a man with 2 minutes IELT could present with a perception of poor control over his ejaculation, distressed about his condition, has interpersonal difficulties and therefore be diagnosed with PE

Premature ejaculation(PE), also known as rapid ejaculation, rapid climax, premature climax or early ejaculation, is the most common sexual problem in men, affecting 25%-40% of men. IT is characterized by a lack of voluntary control over ejaculation.

Masters and Johnson stated that a man suffers from premature ejaculation if he ejaculates before his sex partner achieves orgasm in more than fifty percent of their sexual encounters.

Other sex researchers have defined premature ejaculation as occurring if the man ejaculates within two minutes of penetration.

However, a survey by Alfred Kinsey in the 1950s demonstrated that three-quarters of men ejaculate within two minutes of penetration in over half of their sexual encounters.

Today, most sex therapists understand premature ejaculation as occurring when a lack of ejaculatory control interferes with sexual or emotional well-being in one or both partners.

1.) All women > 65 yrs regardless of additional risk factors.

2.) All women < 65 yrs with one or more risk factors (already discussed). 3.) All postmenopausal women with a fracture. 4.) All women undergoing prolonged hormone therapy. 5.) All men over 70 yrs of age, regardless of additional risk factors. 6.) All men < 70 yrs with one or more risk factors e.g. heavy smoking/ exercise/ alcohol/hypogonadism. In the next issue of KUC Times, we shall discuss the management of Osteoporosis.

The DEXA measures bone density. Bone density has a direct bearing on the risk of fracture.
Treatment improves bone density and reduces fracture risk.

Take a detailed history and identify the risk factors :

1.) Family History – History of osteoporosis.
-Body weight
-History of fracture
-History of renal stone

2.) Medical history

-Reproductive History
Age of menarche
Age of menopause

3.) Lifestyle

Smoking etc.

4.) Diet & Supplements

-Frequent dieting
-Calcium deficiency
-Increased caffeine etc.

5.) Current Medications – If any.

Interestingly, by the time plain X-ray shows decreased bone density (osteopenia), it indicates a bone loss of 30-40%, which is not encouraging.
Blood investigations directly have no relation to osteoporosis. Obviously, they have a bearing on other medical problems which this category of patients(i.e elderly) have.

The WHO definition of osteoporosis is based on a non- invasive radiological investigation called “DEXA SCAN”, which is a sensitive indicator of the bone marrow density (BMD). The reports are self-explanatory and place the patient in either of three categories i.e. normal, osteopenic or osteoporotic, which, then helps in planning the treatment, its duration and how aggressive one has to be.
The DEXA is also a very useful tool to monitor treatment.

Unfortunately not. Osteoporosis is largely a silent disease and by the time a patient has severe back pain and stiffness or a fracture after a trivial fall(usually of the spine/hip/wrist), it means she has largely gone undiagnosed.
Thus, it is extremely important for a clinician to know all the risk factors of osteoporosis (refer to part 1&2) Sadly, in India, a majority of the osteoporotic patients are diagnosed after presenting with a fracture or after a loss of height(compression of vertebrae).

1.) Chronic Inactivity

Insufficient physical activity is the single most important risk factor for osteoporosis. This could be due to plain laziness or a forced paralysis after a spinal injury or weightlessness in Astronauts. The issue is, gravity helps, and doing activities resisting gravity strengthens bones!
Interestingly, a lot of research on bone marrow density(BMD) is carried out in space. Remember, astronauts do a lot of research in space but to prevent osteoporosis, they do a special set of exercises as there is no gravity in space !! (Gravity is good !)

2.) Excessive sports in females

May sound paradoxical! But in later life that’s exactly what happens chiefly due to a strict control in diet and weight, causing loss of all body fat(and hence oestrogen storage sites !). The lack of oestrogens then causes irregular menstrual periods or maybe total stoppage of periods. Muscle mass increases with regular exercises and in some cases regular consumption of oral contraceptives does help, but the eventual trade-off is in the negative.

3.) Low body weight

The new fad amongst young ladies! The reality is “slim women, thin bones”. Underweight women have a high risk of fractures, while overweight women are rarely affected by oestrogens since excess weight strengthens bones and excess fat stores oestrogens, the bone strengthening hormone. That does not mean, we are advocating being overweight! Overweight people have more osteoarthritis! We recommend the “ideal” body weight depending on the height/age/sex.

Importantly, if on a diet please supplement with necessary nutrients (all) and strengthen your muscles and bone with exercises.

4.) Low calcium intake over a long-term period

stimulates the parathyroid hormone which in turn releases calcium from the bones causing osteoporosis.

5.) Depression

A chronic state of depression causes osteoporosis indirectly due to
High level of stress hormones
The drugs themselves
Lack of appetite/inadequate nutrition
Reduced physical activity

6.) Cigarette smoking “the bone terrorist”

Nicotine smoking reduces bone marrow density. Men and women who are chronic smokers have a significantly higher rate of vertebral and hip fractures due to osteoporosis.

Various contributing mechanisms are:-

Nicotine inhibits oestrogen secretion, stimulates its breakdown in the liver and also causes early menopause.
Smoking depletes the body of Vit C which is necessary for bone building and it also increases the toxic load of cadmium and lead which interferes with calcium absorption.
Lastly, smoking directly reduces the blood supply of bones and also inhibits osteoblasts, the bone-forming cells.

7.) Excessive Alcohol

Modest alcohol intake(60 ml/day) increases oestradiol concentration and is thus bone protective, but alcoholism increases the risk of osteoporosis substantially. This is due to :

Accompanying poor nutrition
Lower Bodyweight
Hepatic damage
Decreased calcium absorption
Lowered Oestrogen levels
Lowered testosterone levels

Chronic Alcoholics are 5-10 times more prone to fractures!!

8.) Nutritional deficiency

Nutrition is an essential factor in maintaining bone health
Minerals: Calcium- Calcium supply is a lifelong issue. If there is a constantly decreased calcium intake, it stimulates the parathyroid hormone to release calcium from the bones, which maintains the blood calcium level but drains the bones of calcium causing osteoporosis. Phosphorous, Magnesium, Zinc, Manganese, Copper, Boron, and silica are other minerals necessary.
Vitamins D,C,K,B6, B12, Folic acid
Essential fatty acids

Healthy bones require healthy eating habits !!

9.) Hormones

Early menopause (Natural or Surgical) is an important risk factor.
Insufficient testosterone in men leads to early osteoporosis ( as in chronic alcoholism, Anorexia Nervosa, and Hypogonadism).

10.) Medications

Many drugs weaken bones, most importantly steroids (taken for bronchial asthma, allergies, rheumatic, hematological, intestinal, and immunological diseases and post transplantation). A therapy of more than one year is significant.

Some other common drugs are
Lithium (for depression)
Isoniazid ( for tuberculosis)
Carbamazepine/Dilantin( for Convulsions)
Heparin/Warfarin( Anticoagulants)
Antacids containing Aluminium

Tell your doctor if you are already on some medication. It matters!

In the next issue of KUC Times, we shall discuss the clinical symptoms and signs and the relevant investigations needed for an accurate diagnosis of osteoporosis.

Risks you cannot avoid !!

1.) Genetics:- The “peak bone mass” and the subsequent later loss of bone are genetically programmed. Thus, a family history of osteoporotic fracture is a powerful indicator that genetic factors play a role in the development of osteoporosis. There are certain genetic syndromes which can be detected on a careful physical examination (e.g. Turners syndrome, Osteoporosis Imperfecta etc.)

2.) Race :- Caucasian and Scandinavian residents are more prone to osteoporosis.

3.) Sex and Age:- Till the age of 30-35, both bone formation and bone resorption are balanced. Thereafter, the genetically determined bone loss sets in – greater in women than men. With the onset of menopause in women(around 45-50 years) the oestrogen levels fall, thus increasing the rate of osteoporosis and fractures. In men, the risk of fractures increases steadily after 75 years.

4.) Previous fractures:- A single spontaneous vertebral fracture raises the risk of further vertebral fractures by a factor of 5.

5.) Pregnancy and lactation:- In general, there is a transient decrease in bone density during pregnancy and breastfeeding. Despite an increase in sex hormones during pregnancy causing an increased uptake of calcium from the gastrointestinal tract, an inadequate diet will directly drain the skeleton. This problem shall be compounded in case of multiple pregnancies, prolonged lactations, poor nutrition and no calcium and Vit D3 supplements during these periods. The weeks of bed rest with every pregnancy further aggravates osteoporosis.

Until recently, the diagnosis of Osteoporosis was made only when the patient presented with a fracture !! Today we realize that recognizing and avoiding risk factors, prevents many chronic illnesses. Osteoporosis is not an exception and it has avoidable and some unavoidable risk factors.

1. A better understanding of bone as a dynamic organ and methods to delay/ halt bone loss.

2. Failing to realize that osteoporosis is not a “normal”, relatively unimportant aspect of aging.

3. An increasingly aging population chiefly due to better health delivery systems.

4. Lack of obvious signs and symptoms in osteoporosis (the silent thief!).

5. Poor demarcation among health professionals as to who should treat, when to start treating, how to diagnose, how long to treat, etc.

6. Poor education/ knowledge among the society about osteoporosis and its potentially alarming range of possible complications.

7. Economics of osteoporosis prevention, detection, treatment is huge. Even more expensive is treating the complications of osteoporosis e.g. a hip fracture.

8. Lastly, waiting and expecting action from other clinicians rather than informing yourself about all aspects of osteoporosis and initiating treatment yourself.

1. Along with hypertension and diabetes, osteoporosis is now identified as one of the most important diseases affecting the human race.

2. Osteoporotic fractures affect more women than heart attacks, strokes and all female cancers combined.

3. 50% of patients with osteoporosis and hip fractures lose their independence. In the new millennium, it is totally unacceptable that half of all post menopausal women should suffer fractures when these can be avoided by adequate preventive measures.

Simply because of the correlation of low bone density with fracture risk. Treating low bone density makes plain common sense. In fact, this low bone density as a fracture risk has a better correlation than high cholesterol to Heart attack risk or high blood pressure to a stroke risk !!

The commonest myths are :
I am too young to get osteoporosis
Only women get osteoporosis
I drink a lot of milk and therefore I won’t get osteoporosis.
My mother had osteoporosis and so I am doomed to have it.
I will know when I get it.

All Myths!

Quite simply put, Osteoporosis is a skeletal disorder characterized by compromised bone strength predisposing to an increased risk of fracture. According to the WHO, osteoporosis is defined in terms of bone density measurement on a DEXA Scan as a bone mass of more than 2.5 standard deviations (SD) below that of healthy premenopausal adult females, (called the T-score).

Varicoceles causing only pain and discomfort are treated by non-operative measures like – scrotal support; cold douches and analgesics. If symptoms do not respond, then surgical treatment is necessary.

Different types of surgical interventions are possible open varicocelectomy, laparoscopic varicocele ligation and microsurgical ligation. The success rates are the highest with microsurgery with less than 1% recurrence and complications. The other techniques have a higher recurrence rate up to 10% and are largely abandoned now. The microscopic procedure requires single day admission and a quick return to work due to it’s very small incision. The results of varicocele surgery for infertility patients are good with pregnancy rate of 60% after 9 to 12 months after surgery.

The exact mechanism of varicocele causing infertility is uncertain but varicocele increases the temperature of scrotum due to poor drainage of veins and this suppresses sperm production. Some believe that a gonadotoxin is present in such patients which explains why the opposite testis is also affected in a unilateral varicocele.

Many patients with varicoceles have abnormal semen analysis so this must be done even in young unmarried adults as well. Varicoceles with normal semen analysis can be treated for pain.

Symptoms of varicocele are heaviness or a dragging pain in the scrotum usually on the left side; smaller size of testicle on the affected side; infertility and palpable or visible swelling on the affected side of both sides.

A good clinical examination with valsalva manouvre can diagnose most varicoceles. A Doppler ultrasound can pick up small 2mm or more sizes veins and confirm reflux.

Varicocele is usually idiopathic, and the basic fault lies in the valves of the veins that become leaky, allowing blood to reflux back towards testis. A secondary varicocele in a male more than 40 years of age warrants search for a cause like malignancy.

Varicocele is an abnormal dilatation of testicular veins. It causes reflux and stasis in these veins and can have an adverse impact on the male fertility. It is usually found in about 15-20% of young adult males. 40% of patients presenting with infertility have a varicocele.

UDS is usually offered to patients without a clear cause for their voiding symptoms. It is of great help in patients of stroke, paraplegia and quadriplegia, young children with incontinence and women with incontinence, long-standing diabetes with retention of urine and patients of other CNS disorders like Parkinsonism. Many elderly patients can be saved from unnecessary surgery as UDS clearly tells whether they have obstruction due to prostate or not.

Though the technique appears simple, UDS should be done by a trained urologist who can also interpret the data collected by the computer. A report without interpretation and diagnosis is meaningless.

UDS is a minimally invasive test that is done on outpatient basis. Small catheters are introduced into the bladder under local anesthesia and a small balloon in the stool passage to measure bladder abdominal pressures. The Bladder is filled with saline and pressures measured by computer using transducers. Data is collected in a preloaded format.

UDS is important in patients who complain of incontinence, urgency and frequency without clear-cut obstruction to flow. It measures the bladder pressures during filling and voiding which is not possible with any other imaging technique. It helps avoid unnecessary surgeries on lower tract.

Urodynamic study is an objective assessment of the bladder function of both during storing as well as voiding of urine. It tells about the abnormalities of lower urinary tract when a patient complains of voiding difficulty.

It is always conservative to start with.
1.) Activity modification/trigger prevention.
2.) Rehabilitation protocol that emphasis patello femoral control rather than pure quadriceps strengthening.
3.) Occasionally bracing/correction of associated foot deformities if present.
4.) Non-steroidal anti-inflammatory drug (NS AIDS).
5.) Surgical intervention is rarely indicated and usually consists of a lateral retinacular release to decompress the patello femoral joint, followed by rehabitilization. No surgery can “cure” the primary anatomical anomaly.

The history is classic. The paucity of physical findings is obvious, except for the listed ones. The radiology( Ap/Lateral/Skyline) may pick up some of the anatomical aberrations as listed earlier.

Classically, none except for the anatomical; factors as discussed earlier i.e Flat feet, Genu valgum, position of patella( high, low or lateral), subluxating patella, torsional deformity of femur and/or tibia and finally wasting of vastus lateralis/medialis.

1.) Pain around the anterior aspect of the knee, which increases by the posture of prolonged knee bending or by going upstairs/downstairs.
2.) With instability, you get a feeling of giving way.

As painful or instability syndromes or both.

1.) The commonest trigger is a repetitive overuse, as seen in the sporting activities like running, jumping, swimming, biking, etc
2.) A direct trauma to the front of the knee.
3.) A trauma to the side of the knee causing a patellar subluxation/dislocation. This can trigger off a chronic patello femoral joint problem.

Not necessarily, these pre-dispositions usually lie dormant unless triggered. Thus there are triggers that create clinical complaints from asymptomatic pre-dispositions.

1.) Lack of / weak vastus medialis obliquus muscle causing a relative overactivity of the vastus lateralis muscle.
2.) An overdeveloped Vastus lateralis muscle.
3.) An increase in Quadriceps angle.
4.) A tight lateral retinaculum.
5.) A flat foot from soft tissue causes.

1.) Excessive rotational/torsional deformity of the femur / and/or tibia.

2.) A high or a low lying patella.
3.) A shallow femoral troclear groove for patellar articulation.
4.) A flat foot from bony causes causing excessive strain on the medical patello femoral joint.

Majority of patello femoral joint problems are related to inherent anatomical factors of this joint. These anatomical factors could be bony or soft tissue. Sadly, a sizeable majority of the general population have these inherent physical predispositions.

Quite interestingly the commonest knee problems are related to the patello femoral joint. And these are more to do with repetitive minor trauma or overuse, rather than a single injury or insult.