Friday, June 24, 2011



One of the most common types of arthritis is osteoarthritis. It has become a leading factor of disability in elderly. In western countries, due to increasing prevalence of obese people as well as aging population, the occurrence of OA is on the rise.

Basically, OA prefers certain joints such as cervical and lumbosacral joint of the spine, hip, knee, first metatarsal phalangeal joint, proximal and distal joint and the base of the thumb whilst other joints such as ankle, wrist and elbow are spared. Ankle cartilage is unique because it is designed to be resistant to loading stress. The joints affected by OA are related to the amount of stress that is placed on them. Knee for example is important as weight bearing joints.

The clinical diagnosis is made on the basis of structural abnormalities or symptoms present. There are many people with abnormal structural finding in radiologic examination but appear to be asymptomatic. This situation is no more important than people with symptomatic OA.

Basically the prevalence of knee OA is higher than hip OA which is account for one third of the cases of knee OA. Some elderly with the appearance of bony prominent in affected hand joints together with radiographic findings of hand OA do not present with any symptoms.

The prevalence of OA is higher as aging process continues. The prevalence of OA in people who are above 60 is prominently higher than those under 40. Gender also plays a role in OA development. It is seems that women has higher risk of OA than men.


OA is defined as joint failure. The disease involves the pathologic changes in all structures of joints although not all parts of the joint are equally affected. This is initiated by hyaline articular cartilage loss. This event is proceed by thickening and sclerosis of subchondral bony plate, by outgrowth of osteophytes at the joint margin as well as by stretching of articular capsule, by weakness of muscles that bridging the joint and by mild synovitis in many affected joints.


a. Joint capsule
b. Ligaments
c. Muscle
d. Tendon
e. Sensory afferent
f. Underlying bone

Joint capsule and ligaments is important as protector as they provide limitation to excursion and range of motion. Ligaments along with tendons and overlying skin contain mechanoreceptor that is important to provide afferent input to spinal cord so that, the effectors which are muscle and tendons can undergo some changes in term of power and acceleration or deceleration according to specific position.

Bone is important as shock-absorber. The synovial fluid between joint is important as lubricant that reduce the friction-induce cartilage wear. This synovial fluid is synthesized by synovial fibroblast and consists of mucinuous glycoprotein, lubricin.

The development of OA increases when one or more joint protectors is failed to work properly. One of the examples is the Charcot’s arthropathy. This occurs due to the presence of posterior column peripheral neuropathy with minor joint injury that can cause severe and rapidly progressive OA.

Cartilage also serves as joint protectors. As mentioned somewhere in the text, this structure is the primary site to be affected in early pathogenesis of OA. Cartilage is aneural. It can be found at the end of bone where it has contact with another bone. Basically, cartilage consists of chondrocytes and matrix. Cartilage matrix is produced by chondrocytes under influence of cytokines and growth factors. The balance between cartilage catabolism and anabolism is regulated by growth hormones, cytokines and mechanical stress.

Cartilage matrix consists of two main macromolecules; collagen type II and aggrecan. Collagen type II provides tensile strength and aggrecan provides compressive stiffness to the cartilage. In normal structure, collagen type II is tightly woven and aggrecan can be found in the matrix interstices between collagen. Aggrecan is proteoglycan that is linked to highly negatively charged hyaluronic acid. Compression in close proximity between collagen creates great electrostatic repulsion that give characteristic of compressive stiffness.

The enzymes produced are important for degradation of cartilage. The major enzymes involve in collagen catabolism is metalloproteinase-13 (MMP-13) or collagenase 3. Other collagenase play minor role. Aggrecan is mainly degraded by aggrecanse 1 (ADAMTS 4) and perhaps of MMPs too. These enzymes usually act at the territorial matrix surrounding chondrocytes but in pathologic process such as in OA, the activity is spread widely across the matrix especially in the superficial layer of cartilage.

Cytokines are also important for regulation of matrix metabolism. The main cytokines is interleukin-1 (IL-1) that has effect on nucleus. It can induce transcriptional process of proteinase while inhibit the synthesis of matrix elements. Tumor necrosis factor α has similar role. These cytokines can induce the synthesis of nitric oxide, prostaglandin E2 and bone morphogenic protein 2 by chondrocytes. These factors are important for metabolism. Nitric oxide can suppress the synthesis of aggrecan and enhances proteinase activity, BMP 2 is a potent anabolic stimulator. The activity of MMPs is regulated by tissue inhibitor of metalloproteinase (TIMP). Growth factors such as transforming growth factor β and insulin-like growth factor type I do play prominent role.


a. Systemic risk factors

Age is the most potent factor for OA. This is due to the decrease in responsiveness of cartilage towards stimulation when we get older. Other than that, other joints protectors also undergo degenerative process. Muscle becomes weaker and slower in response towards oncoming impulse, ligament stretch with age and become less able to absorb impulse. Afferent fibers become slower so that the efferent, muscle and tendon become slower in response towards stimuli due to retardation of the feedback loop of mechanoreceptors. The combination of all factors above acts in concert to increase the vulnerability of the joint to OA.

b. Genetics and heritability

Genetics and heritability have some influence to hands and hip OA. Generalized OA is rarely inherited. There are some evidences related to FRZB gene that is essential to produce Frizzle protein that antagonize extracellular Wnt ligand. Basically Wnt signalling is important for matrix synthesis and joint development.

c. Joint environment

Some risk factors increase the susceptibility of joint to focal stress. Congenital dysplasia, Legg-Perthes disease, and slipped femoral capital epiphysis are three uncommon developmental abnormalities occurring in utero or childhood can leave the child with future OA. Acetabular dysplasia is more common in girls whilst others are more dominant in boys.

Major injuries can also lead to OA because it can produce structural abnormalities. This theory explains the occurrence of OA in joints such as ankle and wrist that are otherwise rare.

Furthermore, tears of ligament such as anterior cruciate ligament of the knee or the labrum of the hip can increase the risk of OA later in life. The operation such as menisectomy that is carried out as a result of the tear has independent risk of developing OA with the injury itself.

Malalignment is another risk factor. There are two forms of malalignment. Varus knee is the bowlegged knee in which the focal stress increase highly in the medial or interior compartment while the Valgus (knock knee) has predispotion of lateral compartment cartilage damage. As a result of this malalignment cartilage loss and/or bone damage can occur.

d. Loading Factors

Loading factors here include obesity and repetitive joint use. Obesity usually precedes OA. Basically, there is an increase risk in knee OA in obese people because the increase in body weight would increase load on the joint especially on the weight bearing joint. On single stance during walking, three to six times of body weight would be exerted across the knee joint. Women has stronger risk factor than men. In women, there is a linear relationship between the weight and the risk of OA. Hip OA can also develop but less than knee. Hands OA is modestly related to obese people that might be contributed by other factor such as metabolic factor.

The repeated use of joint can be further divided into occupational use and leisure time physical activities. Basically, the risk of OA for occupational use is specific to the joint involves in occupation. The examples of these include farmer who might contract hip OA, miners are more prone to develop knee and spine OA whilst shipyard or dockyard workers might have increased risk of fingers and knees OA. Muscle that is use for a long period of time during working hours may become weaker and exhausted with time. So, the effectiveness of muscle as one of joint protectors is reduced. Exercise is one of the treatments of OA, but certain types of exercise do increase the risk of OA.


Pain in OA is related to activity. Activity always initiates the pain and may be resolved slowly when we take a rest. Pain can be episodic in early cases of OA or persistent as disease progresses. Stiffness may be prominent but morning stiffness maybe brief (less than 30 minutes) as compared to inflammatory arthritis. Buckling may occur in knees due to muscle weakness that cross the joints. Chronic knee pain in people above 45 have long differential diagnoses. Anserine bursitis (medial and distal to the knee) and inflammatory arthritis are the common causes of knee OA. Routine blood tests are not indicated for OA. Synovial fluid analysis is helpful. In inflammatory arthritis, gout and pseudogout, we can find white blood count > 1000 microliter. The last two diseases mentioned are also accompanied by crystals findings. X-ray is only needed in chronic hand pain or hip pain. The necessity of radiograph exam for knee pain is indicated when atypical signs and symptoms presence or when the effective treatment is failed.


The therapy of OA can be divided into pharmacotherapy and non-pharmacotherapy. The aim of the therapy is to manage pain and minimize loss of physical function.

a. Non-pharmacology therapy

Basically, some of the intervention can be taken in order to reduce focal load on joint such as avoiding activities that overload the joint, strengthening and conditioning muscle that bridging the joint and unloading the joint by using a cane, a splint, a crutch, or a brace to redistribute the load. Moreover, exercise is one of the effective therapies for at least knee OA. Exercise can strengthen muscle that is one of joint protectors. The more suitable type of exercise is isokinetic and isotonic strengthening exercise that involve the extension or the flexion of the knee against resistance. Moreover, exercise helps in reducing weight, so, the loading factor can be reduced. In the case of OA, muscle usually become weaker due to aging that decrease muscle strength, disuse muscle atrophy due to immobility, alteration of gait to lessen focal load that lead to disuse muscle as well as arthrogenous inhibition due to the joint capsule stretched that inhibit mechanoreceptor feedback loop.
Other physical measures that can be tried are hydrotherapy, local heat, ice packs and massage.

b. Pharmacotherapy

Acetaminophen, NSAIDs and aspirin can be used to treat OA pain. Sometimes, acetaminophen alone is adequate for the patient. In most of the case, NSAIDs is widely used but give different results to consumers. Basically, NSAIDs should be taken on ‘as needed’ medication but when the disease become ineffective to be managed, daily dosing is indicated. However, this drug should be taken with caution because it has many side effects including the life-threatening complications. One of the common side effects is gastrointestinal toxicity that includes dyspepsia, nausea, bloating, GI bleeding and ulcer. Precaution of NSAIDs such as take right after meal, avoidance from taking two NSAIDs, usage of safer NSAIDs such as ibuprofen and nabumetone as well as the use of gastroprotective agent for high risk patient. In addition, NSAIDs can also lead to oedema and renal insufficiency because of the prostaglandin inhibition of afferent blood supply to glomeruli in the kidneys. Selective COX-2 inhibitor is available with less GI side effect but increased cardiovascular side effect. This can lead to inhibition of prostaglandin I2 synthesis in vascular endothelial cells but not in the platelets. This can precipitate stroke or myocardial infarction due to increased risk of intravascular thrombosis.

c. Intra-articular injection

Two kinds of injection can be given according to indication. Glucocorticoids can be injected in patient in acute flares of pain that provide relief for only about 1 – 2 weeks because of the presence of loading or vulnerability joint factors. Hyaluronic acid treatment is still controversial.

d. Surgery

Basically, there are many types of surgery that can be performed in order to correct deformity produced by the effect of OA. This includes osteotomy. In osteotomy, the realignment of the joint if performed to unload excessive load in arthritic joint. On the orther hand, surgeon can also perform arthrodesis, the procedure in which the joint undergoes permanent stiffening by excision and fusion to stop pain. Other than that, arthroplasty either partial or total can be carried out. This procedure involves the artificial replacement of the joints.


1. Fauci AS, Longo DL et al, editors. Osteoarthritis. 17th ed. 2008.
2.Kumar P, Clark M, editors. Osteoarthritis. Kumar and Clark Clinical Medicine, 5th ed.
3. McLatchie G, Borley N, Chikwe J, editors. Osteoarthrosis. Oxford Handbook of Clinical Surgery, 3rd ed, 2007.

Tuesday, June 21, 2011

Life and Expectation I

I went to the hospita at 6.10 a.m today and it was considered as late for Surgery department. I met one resident who asked me about what time I came today. This is the conversation.

Residen: Have you studied about all your patients?
Me: Nope because I went back at 1 a.m in the morning yesterday. I followed another Orthopedic residen to Operation Theater.
Residen: Then, what time you came today?
Me. 6.10 a.m.
Residen: What did you do after that surgery?
Me: Sleep. (for sure I need to sleep because I need to wake up at 5. I just slept for 3 hours only, huhuh)
Residen: You shoud study about your patient ok because......

It is funny for me when I thought again about that. Btw I am not robot and need to recharge to be become energetic but he is right because I need to know my patient in detail and the disease itself so that I won't get blurr when I need to answer my patients question. Thanks a lot my residen :)

Monday, June 6, 2011


I went to one watch shop today in one of new shopping malls in JB. I was greet by the shop owner at that moment. This is our conversation.

Owner: Welcome.
Me: Hi.
Owner: Are you Malay?
Me: Yes.
Owner: Are you Singaporean?
Me: Nope. I am Malaysian.

I went to Oris section then...

Owner: (with smile) Do you like Oris?
Me: (In doubt) Emm.. Yes..

Then I went there and used my eyes to track the models and prices? OMG. My conclusion is:

First - I don't like the model
Second - I think the price is too expensive for me ... heheheh.. I could never afford that ! :)
Third - I don't need to be other than Malay or poss other nationality to buy expensive watch ...

Let's continue with my other story. I would like to thank my parents and siblings for the presents. Btw special goes to my parents and my Sis Fairuz a.k.a. Lush for the lovely presents :) You make my collection become more and more complete for every single year :)

From my parents :

Guess Collection (Gc)

Avon, the brand that we have been using for about 15 years ...

This is special bought for me by my sister, Fairuz @ Lush.. She bought the most expensive present for me that she ever bought for anyone. I really appreciate it :)