Primary vs secondary osteoarthritis

Home | Subscribe | Resources | Reprints | Writers’ Guidelines

February 19, 2007

Coding for Osteoarthritis
For The Record
Vol. 19 No. 4 P. 38

Osteoarthritis is a chronic joint disorder characterized by degeneration of joint cartilage and the adjacent bone. Degeneration occurs due to rubbing of the joint surfaces, causing a wearing away of the tissues. It is the most common type of arthritis and usually occurs in the hands, knees, hips, and spine.

Other common names for osteoarthritis are degenerative arthritis, hypertrophic arthritis, degenerative joint disease, and osteoarthrosis. Osteoarthritis of most sites, except the spine, is assigned to ICD-9-CM category 715. Osteoarthritis of the spine is assigned to category 721. The specific code assignment depends on the site of the spine involved (ie, cervical, thoracic, lumbar) and if myelopathy is present. In category 715, the fifth-digit code assignment identifies the specific site involved. The fourth-digit code assignment identifies whether the osteoarthritis is generalized or localized.

Generalized osteoarthritis (code 715.0x or 715.8x) affects many joints, while localized osteoarthritis affects the joints of one site. Localized osteoarthritis can be further broken down into two other categories: primary and secondary. Primary osteoarthritis (715.1x), also known as idiopathic, affects joints of one site with no known cause. Secondary osteoarthritis (715.2x) affects a joint of one site and is due to some external or internal injury or disease. If the localized osteoarthritis is not specified as primary or secondary, code 715.3x is assigned. Bilateral involvement of the same site is still considered localized and is included in the fifth digit for the site. Code 715.9x is assigned when it is not specified as generalized or localized.

However, it is encouraged not to assign this unspecified code. According to AHA Coding Clinic for ICD-9-CM, when the osteoarthritis “affects only one site but is not identified as primary or secondary, it is coded to 715.3x.” In addition, AHA Coding Clinic for ICD-9-CM goes on to say that “if it involves more than one site but is not specified as generalized, assign code 715.8x” (AHA Coding Clinic for ICD-9-CM, 1995, second quarter, page 5).

Symptoms
The symptoms of osteoarthritis include the following:

• joint pain, which also includes pain of the muscles, ligaments, synovial capsule, and bones around the joint;

• joint stiffness;

• loss in range of motion of affected joints;

• discomfort in joint before or during a change in weather;

• joint swelling; and

• bony lumps in joints of fingers (nodes).

Diagnosis
Osteoarthritis is typically diagnosed based on findings in a physical exam, which includes the description of the symptoms and location and pattern of pain. An x-ray will confirm the diagnosis. Blood tests, computed tomography scans, and MRIs are not used to diagnosis osteoarthritis but may be performed to rule out other types of arthritis. A joint aspiration may also be done to rule out other diseases.

Treatment
Although there is no known cure for osteoarthritis, the goals of treatment include the following:

• relieving pain;

• protecting joints; and

• enhancing joint function.

Medications do not reverse or slow the progression of joint damage, but they do relieve pain, reduce inflammation, and improve stiffness. The following prescription and over-the-counter medications are typically used in the treatment of osteoarthritis:

• pain relievers — acetaminophen (Tylenol), tramadol (Ultram);

• COX-2 inhibitors, which reduce pain and inflammation — Celecoxib (Celebrex);

• topical pain relievers, which can provide temporary arthritis relief — trolamine salicylate (Aspercreme, Sportscreme), methyl salicylate, menthol, and camphor (Icy Hot, Ben-Gay), capsaicin.

• antidepressants, which reduce chronic pain and help depression and insomnia — amitriptyline (Elavil), nortriptyline (Pamelor, Aventyl); and

• injection of pain relievers, which also reduce inflammation —corticosteroid, hyaluronic acid (viscosupplementation).

If the joint can no longer function properly, the patient may require surgery to replace it. Total hip replacement is classified to code 81.51, and partial hip replacement goes to code 81.52. Code 81.54 identifies both partial and total knee replacement. Revision of a joint will go to a different range of codes. According to AHA Coding Clinic for ICD-9-CM, “Any time the joint is replaced or revised after the initial replacement would be considered a revision” (AHA Coding Clinic for ICD-9-CM, second quarter 1996, page 13). The codes for the hip replacement components include the following:

• 00.70, Revision of hip replacement, both acetabular and femoral components;

• 00.71, Revision of hip replacement, acetabular component;

• 00.72, Revision of hip replacement, femoral component; and

• 00.73, Revision of hip replacement, acetabular liner and/or femoral head only.

The codes for the knee replacement components include the following:

• 00.80, Revision of knee replacement, total (all components);

• 00.81, Revision of knee replacement, tibial component;

• 00.82, Revision of knee replacement, femoral component;

• 00.83, Revision of knee replacement, patellar component; and

• 00.84, Revision of total knee replacement, tibial insert (liner).

There is an instructional note under subcategory 00.8 that states, “Report up to two components using 00.81-00.83 to describe revision of knee replacements. If all three components are revised, report 00.80.” In other words, if the tibial and femoral components are revised, assign both code 00.81 and code 00.82.

Coding and sequencing for osteoarthritis are dependent on the physician documentation in the medical record and application of the Official Coding Guidelines for inpatient care. Also, use specific AHA Coding Clinic for ICD-9-CM and American Medical Association CPT Assistant references to ensure complete and accurate coding.

— This information was prepared by Audrey Howard, RHIA, of 3M Consulting Services. 3M Consulting Services is a business of 3M Health Information Systems, a supplier of coding and classification systems to nearly 5,000 healthcare providers. The company and its representatives do not assume any responsibility for reimbursement decisions or claims denials made by providers or payers as the result of the misuse of this coding information. More information about 3M Health Information Systems is available at www.3mhis.com or by calling 800-367-2447.

What causes osteoarthritis?

Primary osteoarthritis is mostly related to aging. With aging, the water content of the cartilage increases and the protein makeup of cartilage degenerates. Repetitive use of the joints over the years causes damage to the cartilage that leads to joint pain and swelling. Eventually, cartilage begins to degenerate by flaking or forming tiny crevasses. In advanced cases, there is a total loss of the cartilage cushion between the bones of the joints. Loss of cartilage cushion causes friction between the bones, leading to pain and limitation of joint mobility. Damage to the cartilage can also stimulate new bone outgrowths (spurs) to form around the joints. Osteoarthritis occasionally can be found in multiple members of the same family, implying an heredity (genetic) basis for this condition. Rarely, some of these hereditary cases of osteoarthritis are caused by defects in collagen, which is an important component of cartilage.

Secondary osteoarthritis is caused by another disease or condition. Conditions that can lead to secondary osteoarthritis include obesity, repeated trauma or surgery to the joint structures, abnormal joints at birth (congenital abnormalities), gout, rheumatoid arthritis, diabetes, and other hormone disorders.

Obesity causes osteoarthritis by increasing the mechanical stress on the cartilage. In fact, next to aging, obesity is the most powerful risk factor for osteoarthritis of the knees. The early development of osteoarthritis of the knees among weight lifters is believed to be in part due to their high body weight. Repeated trauma to joint tissues (ligaments, bones, and cartilage) is believed to lead to early osteoarthritis of the knees in soccer players. Interestingly, recent studies have not found an increased risk of osteoarthritis in long-distance runners.

Crystal deposits in the cartilage can cause cartilage degeneration, and osteoarthritis. Uric acid crystals cause arthritis in gout, while calcium pyrophosphate crystals cause arthritis in pseudogout.

Rheumatoid arthritis and other inflammatory conditions of the joints lead to joint damage and eventual degeneration of the cartilage and osteoarthritis.

Some people are born with abnormally formed joints (congenital abnormalities) that are vulnerable to mechanical wear, causing early degeneration and loss of joint cartilage. Osteoarthritis of the hip joints is commonly related to design abnormalities of these joints that had been present since birth.

Hormone disturbances, such as diabetes and growth hormone disorders, are also associated with early cartilage wear and secondary osteoarthritis.

Osteoarthritis

What is osteoarthritis?

Osteoarthritis, also known as degenerative joint disease (DJD), is the most common type of arthritis. Osteoarthritis is more likely to develop as people age. The changes in osteoarthritis usually occur slowly over many years, though there are occasional exceptions. Inflammation and injury to the joint cause bony changes, deterioration of tendons and ligaments and a breakdown of cartilage, resulting in pain, swelling, and deformity of the joint.

There are two main types of osteoarthritis:

  • Primary: Most common, generalized, primarily affects the fingers, thumbs, spine, hips, knees, and the great (big) toes.
  • Secondary: Occurs with a pre-existing joint abnormality, including injury or trauma, such as repetitive or sports-related; inflammatory arthritis, such as rheumatoid, psoriatic, or gout; infectious arthritis; genetic joint disorders, such as Ehlers-Danlos (also known as hypermobility or “double-jointed; congenital joint disorders; or metabolic joint disorders.

What is cartilage?

Cartilage is a firm, rubbery, flexible connective tissue covering the ends of bones in normal joints. It is primarily made up of water and proteins whose primary function is to reduce friction in the joints and serve as a “shock absorber.” The shock-absorbing quality of normal cartilage comes from its ability to change shape when compressed, because of its high water content. Although cartilage may undergo some repair when damaged, the body does not grow new cartilage after injury. Cartilage is avascular, meaning there are no blood vessels in it. Therefore, healing is a slow process.

Cartilage is made up of two main elements: cells within it known as chondrocytes and a gel-like substance called matrix, composed mostly of water and two types of proteins (collagen and proteoglycans).

  • Chondrocytes, and the precursor form chondroblasts, are highly complex multifunctional cartilage cells. Functions include synthesizing and maintaining the extracellular matrix comprised of collagen and proteoglycans that help healthy cartilage grow and heal.
  • Collagen is a structural protein found in many tissues such as skin, tendons and bone and is a key structural component of cartilage. Collagen provides cartilage with its strength and creates a framework for the other components.
  • Proteoglycans are complex molecules composed of protein and sugar combinations that are interwoven in the matrix of cartilage. Their function is to trap large amounts of water in cartilage, which allows it to change shape when compressed thus acting as a shock absorber. At the same time, proteoglycans repel each other, allowing cartilage the ability to maintain its shape and resilience.

Who is affected by osteoarthritis?

Approximately 80% of older adults, ages 55 years and older, have evidence of osteoarthritis on X-ray. Of these, an estimated 60% experience symptoms. It is estimated that 240 million adults worldwide have symptomatic osteoarthritis, including more than 30 million U.S. adults. Post-menopausal women have an increased incidence of knee osteoarthritis compared to men.

Are there other risk factors for osteoarthritis?

In addition to age and secondary causes such as inflammatory arthritis and prior injury/ trauma, several other risk factors increase the chance of developing osteoarthritis including obesity, diabetes, elevated cholesterol, sex, and genetics.

  • Obesity is a risk factor for osteoarthritis, particularly of the knee. In addition to overloading the weight-bearing mechanisms of the body, the metabolic and pro-inflammatory effects of obesity have been studied as contributory to osteoarthritis. Maintaining ideal body weight or losing extra weight is important for those at risk.
  • Both diabetes and hyperlipidemia (elevated lipids/cholesterol) contribute to the inflammatory response within the body, increasing the risk of osteoarthritis. Oxidation of lipids can also create deposits in cartilage which affects affecting blood flow of subchondral bone in the same way that blood vessels are affected by atherosclerosis. Elevated blood sugars, as well as elevated cholesterol/lipids, increase free radicals within the body, this oxidative stress exceeds the resilience of cartilage on the cellular level. Controlling diabetes and hyperlipidemia is important for bone health in addition to general health.
  • Decreased estrogen as experienced by post-menopausal women increases the risk of knee osteoarthritis as estrogen is protective of bone health specifically reducing oxidative stress to the cartilage.
  • Heredity can play a role in osteoarthritis, as individuals born with other bone diseases or genetic traits may be more likely to develop osteoarthritis. For example, Ehlers-Danlos, which is characterized by joint laxity or hypermobility, can contribute to osteoarthritis.

Primary osteoarthritis is a heterogeneous disease meaning it has many different causes, it is not only “wear and tear” arthritis. Some contributing factors to OA are modifiable (can be changed) and others are non-modifiable (cannot be changed such as born with it or now permanent). Age is a contributing factor, although not all older adults develop osteoarthritis and for those who do, not all develop associated pain. As discussed above, there can also be inflammatory and metabolic risks that can increase the incidence of osteoarthritis, particularly in the setting of diabetes and/or elevated cholesterol.

Osteoarthritis can be genetic both as primary such as nodular OA of the hands as well as secondary related to other genetic disorders, such as hypermobility of joints. Inflammatory and infectious arthritis can contribute to the development of secondary osteoarthritis due to chronic inflammation and joint destruction. Previous injuries or traumas including sports-related and repetitive motions can also contribute to osteoarthritis.

Although the exact mechanisms of cartilage loss and bone changes are unknown, advancements have been made in recent years. It is suspected that complex signaling processes, during joint inflammation and defective repair mechanisms in response to injury, gradually wear down cartilage within the joints. Other changes cause the joint to lose mobility and function, resulting in joint pain with activity.

Share Facebook Twitter LinkedIn Email Get useful, helpful and relevant health + wellness information enews

Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Policy

What is Osteoarthritis?

Osteoarthritis is the most commonly diagnosed type of joint arthritis disease, which can affect hands, knees and hips. Knee arthritis is known to affect joint functionality causing knee pain and even leading to disability as it progresses. There are different stages of knee osteoarthritis, with 0 assigned to a normal, healthy knee right up to the advanced stage 4 that is severe OA.

The Center for Disease Control and Prevention has found that the number of people suffering from knee pain disorder is gradually rising, with approximately 1 in 2 people likely to develop symptomatic knee OA in their lifetime leading to significant impact on health, workplace productivity and economic costs.

OA pain is easily identifiable through diagnostics and common symptoms. Some people who suffer from immense osteoarthritis knee pain may only show mild changes on x-ray, so it is extremely important to concentrate on the symptoms, rather than just the x-rays. Here is a look at the stages of osteoarthritis of the knee ranging from normal, minor, mild, moderate and severe stages, with appropriate treatment plans.

Stage 0- Normal

When the knee shows no signs of osteoarthritis, it is classified as Stage 0, which is normal knee health, with no known impairment or signs of joint damage.

Treatments

There is no treatment required for stage 0 OA.

Stage 1- Minor

Stage 1 OA patients will develop very minor wear & tear and bone spur growths at the end of the knee joints. However, at this stage it is unlikely you will feel pain or discomfort.

Treatments

If the patient is not predisposed to OA, orthopedic physicians may not recommend any special treatment for stage 1. However, supplements such as glucosamine and chondroitin may be recommended. Lifestyle considerations like regular exercise may also prove to be helpful.

Stage 2-Mild

In Stage 2, diagnostic images or X-rays of knee joints will show more bone spur growth, and though the space between the bones appear normal, people will begin experiencing symptoms of joint pain. Typically, the area around the knee joints will feel stiff and uncomfortable, particularly when sitting for an extended period, after rising in the morning, or after a workout. Though the cartilage and soft tissues remains at a healthy size, there is proteolytic breakdown of the cartilage matrix from an increased production of enzymes, such as metalloproteinases.

Treatments

When your physician detects and diagnoses OA at this early stage, it is easier to follow a plan to stop the progression of this joint disease. There are different nonpharmacologic therapies to help relieve the pain and discomfort caused in this mild stage. Many patients are recommended a strict regimen of exercise and strength training for increased joint stability. Additionally, braces, knee supports or shoe inserts may be used to protect the knee from stress.

Stage 3- Moderate

Stage 3 is referred to as “moderate”, where there is obvious erosion to the cartilage surface between bones and fibrillation narrows the gap between the bones. There are proteoglycan and collagen fragments released into the synovial fluid as the disease progresses, wherein the bones develop spurs at the joints as it becomes rougher.

With the progression of osteoarthritis of the knee, there is obvious joint inflammation which causes frequent pain when walking, running, squatting, extending or kneeling. Along with joint stiffness after sitting for long or when waking up in the morning, there may be popping or snapping sounds when walking.

Treatments

Over the counter NSAIDs or pain-relief therapies may be prescribed. If these methods are not effective, the orthopedic doctor may prescribe stronger pain medicine, such as codeine and oxycodone.

Patients that have not responded positively to physical therapy, weight loss program, use of NSAIDs may require viscosupplementation, which are intra-articular injections of hyaluronic acid into the knee joint. Moderate knee arthritis can be treated aggressively with three to five injections of hyaluronic acid over 3-5 weeks’ time, which may take several weeks for the treatment to start showing results, but pain relief typically lasts six months.

Stage 4- Severe

Stage 4 is considered to be severe. In stage 4 the joint space between the bones are considerably reduced, causing the cartilage to wear off, leaving the joint stiff. The breakdown of cartilage leads to a chronic inflammatory response, with decreased synovial fluid that causes friction, greater pain and discomfort when walking or moving the joint.

There is increased production of synovial metalloproteinases, cytokines and TNF that can diffuse back into the cartilage to destroy soft tissue around the knee. The advanced stage of the disease shows development of more spurs causing excruciating pain, which makes even everyday chores, including walking and descending stairs a challenge.

Treatments

In cases of severe OA of the knee, an option is performing osteotomy or bone realignment surgery, wherein the orthopedic surgeon cuts the bone above or below the knee to shorten the length and help realign it for less stress on the knee joint. This surgery helps protect the knee by shifting the weight of the body away from the site of the bone spur growth and bone damage.

Another surgical option is total knee replacement, or arthroplasty. During this surgical procedure, the damaged joint is removed and replaced with a plastic or metal prosthesis device. Recovery from surgery may take several weeks and requires patience and discipline, with continuous physical and occupational therapy to regain full mobility.

If you are suffering from knee pain, contact an IBJI physician for a proper diagnosis and treatment plan. The Illinois Bone & Joint Institute has more than 90 orthopedic physicians, and 20 locations throughout Chicago.

What can we do about osteoarthritis?

  1. 1.

    Murray CJL, Lopez AD: The Global Burden of Disease. Boston: Harvard University Press. 1996

    • Google Scholar
  2. 2.

    Consensus document: The Bone and Joint Decade 2000-2010 for prevention and treatment of musculo-skeletal disorders. Acta Orthop Scand. 1998, 69 (suppl 281): 67-86.

    • Google Scholar
  3. 3.

    Kellgren JH, Lawrence JS, Bier F: Genetics factors in generalised osteoarthritis. Ann Rheum Dis. 1963, 22: 237-255.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  4. 4.

    Anderson J, Felson DT: Factors associated with osteoarthritis of the knee in the First National Health and Nutrition Examination Survey (NHANES 1). Am J Epidemiol. 1988, 128: 179-189.

    • PubMed
    • Google Scholar
  5. 5.

    Spector TD, Cicuttini F, Baker J, Loughlin J, Hart DJ: Genetic influences on osteoarthritis: a twin study. Br Med J. 1996, 312: 940-944.

    • Article
    • Google Scholar
  6. 6.

    Chitnavis J, Sinsheimer JS, Clipsham K: Genetic influences in end-stage osteoarthritis. Sibling risks of hip and knee replacement for idiopathic osteoarthritis. J Bone Joint Surg Br. 1997, 79: 660-664.

    • PubMed
    • Article
    • Google Scholar
  7. 7.

    Felson DT, Couropmitree NN, Chaisson CE: Evidence for a Mendelian gene in a segregation analysis of generalized radiographic osteoarthritis. The Framingham Study. Arthritis Rheum. 1998, 41: 1064-1071.

    • PubMed
    • Article
    • Google Scholar
  8. 8.

    Hirsch R, Lethbridge-Cejku M, Hanson R: Familial aggregation of osteoarthritis. Data from the Baltimore longitudinal study on aging. Arthritis Rheum. 1998, 41: 1227-1232.

    • PubMed
    • Article
    • Google Scholar
  9. 9.

    Holderbaum D, Haqqi TM, Moskowitz RW: Genetics and osteoarthritis. Arthritis Rheum. 1999, 42: 397-405.

    • PubMed
    • Article
    • Google Scholar
  10. 10.

    Cicuttini MF, Spector DM: The genetics of osteoarthritis. J Clin Pathol. 1996, 49: 617-619.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  11. 11.

    Jimenez SA, Williams CJ, Karasick D: Hereditary osteoarthritis. In: Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford University Press: Oxford,. 1998, 31-49.

    • Google Scholar
  12. 12.

    Palotie A, Vaisanen P, Ott J: Predisposition to familial osteoarthritis linked to type II collagen gene. Lancet . 1989, i: 924-927.

    • Article
    • Google Scholar
  13. 13.

    Ala-Kokko L, Baldwin CT, Moskowitz RW, Prockop DJ: A single base mutation in the type II procollagen gene (COL2AI) as cause of primary osteoarthritis associated with mild chondrodysplasia. Proc Natl Acad Sci USA. 1990, 87: 6565-6568.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  14. 14.

    Pun YL, Moskowitz RW, Lie S: Clinical correlations of osteoarthritis associated with a single-base mutation (arginine519 to cysteine) in type II procollagen gene. A newly defined pathogenesis. Arthritis Rheum. 1994, 37: 264-269.

    • PubMed
    • Article
    • Google Scholar
  15. 15.

    Ritvaniemi P, Korkko J, Bonaventure J: Identification of COLA2I gene mutation in patients with chondrodysplasias and familial osteoarthritis. Arthritis Rheum. 1995, 38: 999-1004.

    • PubMed
    • Article
    • Google Scholar
  16. 16.

    Bleasel JF, Bisagnifaure A, Holderbaum D: Type II procollagen gene (COL2A1) mutation in exon 11 associated with spondyloepiphyseal dysplasia; tall stature and precocious osteoarthritis. J Rheumatol. 1995, 22: 255-261.

    • PubMed
    • Google Scholar
  17. 17.

    Bleasel JF, Holderbaum D, Mallock V: Hereditary osteoarthritis with mild spondyloepiphyseal dysplasia: are there ‘hot spots’ on COL2A1?. J Rheumatol. 1996, 23: 1594-1598.

    • PubMed
    • Google Scholar
  18. 18.

    Bleasel JF, Holderbaum D, Brancolini V: Five families with arginine 519-cysteine mutation in COL2A1: evidence for three distinct founders. Hum Mutat. 1998, 12: 172-176. 10.1002/(SICI)1098-1004(1998)12:3<172::AID-HUMU4>3.0.CO;2-J.

    • PubMed
    • Article
    • Google Scholar
  19. 19.

    Briggs MD, Hoffman SMG, King LM: Pseudoachondroplasia and multiple epiphyseal dysplasia due to mutations in the cartilage oligomeric matrix protein gene. Nature Genet. 1995, 10: 330-336.

    • PubMed
    • Article
    • Google Scholar
  20. 20.

    Meulenbelt I, Bijkerk C, de Wildt SC: Investigation of the association of the CRTM and CRTL1 genes with radiographically evident osteoarthritis in subjects from the Rotterdam study. Arthritis Rheum. 1997, 40: 1760-1765.

    • PubMed
    • Article
    • Google Scholar
  21. 21.

    Meulenbelt I, Bijkerk C, Miedema HS: A genetic association study of the IGF-1 gene and radiological osteoarthritis in a population-based cohort study (the Rotterdam study). Ann Rheum Dis. 1998, 57: 371-374.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  22. 22.

    Horton WE, Lethbridge-Cejku M, Hochberg MC: An association between an aggrecan polymorphic allele and bilateral hand osteoarthritis in elderly white men; data from the Baltimore Longitudinal Study of Aging (BLSA). Osteoarthritis Cartilage. 1998, 6: 245-251.

    • PubMed
    • Article
    • Google Scholar
  23. 23.

    Loughlin J, Irven C, Ferguson C, Sykes B: Sibling pair analysis shows no linkage of generalized osteoarthritis to the loci encoding type II collagen, cartilage link protein or cartilage matrix protein. Br J Rheumatol. 1994, 33: 1103-1106.

    • PubMed
    • Article
    • Google Scholar
  24. 24.

    Chapman K, Mustafa Z, Irven C: Osteoarthritis-susceptibility locus on chromosome 11 q, detected by linkage. Am J Hum Genet. 1999, 65: 167-174.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  25. 25.

    Leppävuori J, Kujala U, Kinnunen J: Genome scan for predisposing loci for distal interphalangeal joint osteoarthritis: evidence for a locus on 2q. Am J Hum Genet. 1999, 65: 1060-1067.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  26. 26.

    Loughlin J, Mustafa Z, Irven C: Stratification analysis of an osteoarthritis genome screen suggestive of linkage to chromosomes 4, 6, and 16. Am J Hum Genet. 1999, 65: 1795-1798.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  27. 27.

    Felson DT: Epidemiology of osteoarthritis. In Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford: Oxford University Press,. 1998, 13-22.

    • Google Scholar
  28. 28.

    McAlindon T, Zhang Y, Hanna M: Are risk factors for patellofemoral and tibiofemoral knee osteoarthritis different? . J Rheumatol. 1996, 23: 332-337.

    • PubMed
    • Google Scholar
  29. 29.

    Felson DT, Zhang Y, Hannan MT: Risk factors for incident radiographic knee osteoarthritis in the elderly. Arthritis Rheum. 1997, 40: 728-733.

    • PubMed
    • Article
    • Google Scholar
  30. 30.

    Hart DJ, Doyle DV, Spector TD: Incidence and risk factors for radiographic knee osteoarthritis in middle-aged women. The Chingford study. Arthritis Rheum. 1999, 42: 17-24.

    • PubMed
    • Article
    • Google Scholar
  31. 31.

    Lohmander LS, Roos H: Knee ligament injury, surgery and osteoarthrosis. Truth or consequences?. Acta Orthop Scand. 1994, 65: 605-609.

    • PubMed
    • Article
    • Google Scholar
  32. 32.

    Roos H, Laurén M, Adalberth T: Knee osteoarthritis after meniscectomy: prevalence of radiographic changes after twentyone years, compared with matched controls. Arthritis Rheum. 1998, 41: 687-693.

    • PubMed
    • Article
    • Google Scholar
  33. 33.

    Spector TD, Dacre JE, Harris PA, Huskisson EC: Radiological progression of osteoarthritis: an 11 year follow up study of the knee. Ann Rheum Dis. 1992, 51: 1107-1110.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  34. 34.

    Dieppe PA, Cushnaghan J, Shepstone L: The Bristol ‘OA500’ Study: progression of osteoarthritis (OA) over 3 years and the relationship between clinical and radiographic changes at the knee joint. Osteoarthritis Cartilage. 1997, 5: 87-97.

    • PubMed
    • Article
    • Google Scholar
  35. 35.

    Dougados M, Gueguen A, Nguyen M: Longitudinal radiologic evaluation of ostearthritis of the knee. J Rheumatol . 1992, 19: 378-384.

    • PubMed
    • Google Scholar
  36. 36.

    Dougados M, Gueguen A, Nguyen M: Radiological progression of hip osteoarthritis: definition, risk factors and correlations with clinical status. Ann Rheum Dis. 1996, 55: 356-362.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  37. 37.

    O’Reilly S, Doherty M: Signs, symptoms, and laboratory tests. In: Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford: Oxford University Press,. 1998, 197-217.

    • Google Scholar
  38. 38.

    Heinegård D, Bayliss M, Lorenzo P: Biochemistry and metabolism of normal and osteoarthritic cartilage. In: Osteoarthritis. Edited by Brandt KD, Doheretty M, Lohmander LS. Oxford: Oxford University Press,. 1998, 74-84.

    • Google Scholar
  39. 39.

    Matyas JR, Ehlers PF, Huang D, Adams ME: The early molecular natural history of experimental osteoarthritis. Arthritis Rheum. 1999, 42: 993-1002.

    • PubMed
    • Article
    • Google Scholar
  40. 40.

    van den Berg WB, van der Kraan PM, van Beuningen HM: Synovial mediators of cartilage damage and repair in osteoarthritis. In:Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford: Oxford University Press,. 1998, 157-167.

    • Google Scholar
  41. 41.

    Amin AR, Attur M, Abramson SB: Nitric oxide synthase and cyclooxygenases: distribution, regulation and intervention in arthritis. Curr Opin Rheum. 1999, 11: 202-209.

    • Article
    • Google Scholar
  42. 42.

    Amin AR: Regulation of tumor necrosis factor-alpha and tumor necrosis factor converting enzyme in human osteoarthritis. Osteoarthritis Cartilage. 1999, 7: 392-394.

    • PubMed
    • Article
    • Google Scholar
  43. 43.

    Grodzinsky AJ, Kim Y-J, Buschmann MD: Response of the chondrocyte to mechanical stimuli. In:Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford: Oxford University Press,. 1998, 123-136.

    • Google Scholar
  44. 44.

    Lark MW, Bayne EK, Flanagan J: Aggrecan degradation in human cartilage. Evidence for both matrix metalloproteinase and aggrecanase activity in normal, osteoarthritic, and rheumatoid joints. J Clin Invest. 1997, 100: 93-106.

    • PubMed
    • PubMed Central
    • Article
    • Google Scholar
  45. 45.

    Sandy JD, Lark MW: Proteolytic degradation of normal and osteoarthritic cartilage matrix. In: Osteoarthritis. 1998, 84-93.

    • Google Scholar
  46. 46.

    Lark MW, Bayne EK, Lohmander LS: Role of stromelysin-1 in cartilage metabolism. In Metalloproteinases as Targets for Anti-inflammatory Drugs. Edited by Bradshaw D, Nixon JS, Bottomley K, Basel: Birkhäuser Verlag,. 1999, 59-83.

    • Google Scholar
  47. 47.

    Tortorella MD, Burn TC, Pratta MA: Purification and cloning of aggrecanase-1: a member of the ADAMTS family of proteins. Science. 1999, 284: 1664-1666. 10.1126/science.284.5420.1664.

    • PubMed
    • Article
    • Google Scholar
  48. 48.

    Rivest C, Liang M: Evaluating outcome in osteoarthrtis for research and clinical practise. In:Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford: Oxford University Press. 1998, 403-414.

    • Google Scholar
  49. 49.

    Hart DJ, Spector TD: Radiographic grading systems. In:Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford: Oxford University Press. 1998, 450-458.

    • Google Scholar
  50. 50.

    Buckland-Wright JC: Quantitation of radiographic changes. In: Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford: Oxford University Press. 1998, 459-472.

    • Google Scholar
  51. 51.

    Peterfy CG: Magnetic resonance imaging. In: Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford: Oxford University Press,. 1998, 473-494.

    • Google Scholar
  52. 52.

    Lohmander LS, Felson DT: Defining and validating the clinical role of molecular markers in osteoarthritis. In: Osteoarthritis. Edited by Brandt KD, Doherty M, Lohmander LS. Oxford: Oxford University Press,. 1998, 519-530.

    • Google Scholar
  53. 53.

    Dieppe P, Chard J, Faulkner A, Lohmander S: Osteoarthritis. In: Clinical Evidence, vol 2. Edited by Godlee F. London: BMJ Publishing Group,. 1999, 437-447.

    • Google Scholar
  54. 54.

    Dieppe P: Osteoarthritis: time to shift the paradigm. Br Med J. 1999, 318: 1299-1230.

    • Article
    • Google Scholar
  55. 55.

    Tanzi RE: A genetic dichotomy model for the inheritance of Alzheimer’s disease and common age-related disorders. J Clin Res . 1999, 104: 1175-1179.

    • Google Scholar
  56. 56.

    Velculescu VE, Madden SL, Zhang L: Analysis of human transcriptomes. Nature Genet. 1999, 23: 387-388.

    • PubMed
    • Article
    • Google Scholar

Understanding the Difference between Primary and Secondary Osteoarthritis

Joint pain, stiffness, grating bones and even tenderness are a few symptoms one suffers when diagnosed with Osteoarthritis. This disease is one of the most common forms of Arthritis. Also known as degenerative joint disease or degenerative arthritis, osteoarthritis affects bone cartilage. As the disease progresses, this cartilage and the cushioning it provides deteriorates. The pain one feels is no different be it primary or secondary osteoarthritis. The main difference between the two lies in what causes them. Let’s take a closer look.

Primary Osteoarthritis: This form of osteoarthritis develops due to aging and the wear and tear that comes along with it. It is not caused by any existing disease and is not due to any injury. Aging increases the water content of the cartilage, in turn gradually decreasing its protein content. When this happen the cartilage begins to flake and develop tiny crevasses. This deterioration causes friction between the bones that leads to pain, inflammation and limitations on joint mobility. This type of osteoarthritis is typically seen in people above the age of 55. It is believed that if we all live long enough, at some point, everybody will be affected by primary osteoarthritis.

Secondary Osteoarthritis: Osteoarthritis in this form develops due to a specific cause such as injury or another disease. It is for this reason that there are more chances of it affecting people at an earlier age. There are a few risk factors that contribute to the onset of the disease.

Obesity: After aging, Obesity is one of the most significant risk factors that cause osteoarthritis. The extra body weight that one has with obesity puts extreme pressure on the joints causing them to deteriorate faster. In fact osteoarthritis of the knee is a very common form of the disease, as the person’s upper body weight bears down on the knees.

Injury: Fractures, ligament tears and repetitive movements, can all lead to the development of osteoarthritis. These injuries have a long-lasting impact, even if you recover from them completely.

Genetics: There are a number of genetic traits that increase the risk of osteoarthritis. Your bone and joint structure are influenced by genetics. Some are born with irregular joint structures that make them more vulnerable to physical wear and tear. In particular there may be a strong correlation between genetics and osteoarthritis of the knee and hip.

Disease: Inflammation from other diseases can increase the risk of developing osteoarthritis. In diseases such as gout, crystal deposits in the cartilage lead to degeneration and osteoarthritis.

Sedentary Lifestyle: Apart from the risk of putting on excess weight, there are other reasons why a sedentary lifestyle can be a contributing factor. The most important being that people who are sedentary tend to have weaker joints and muscles. These weak muscles in turn don’t provide proper support and stability to the joints, leading to early degeneration.

Whether you have primary or secondary osteoarthritis, the treatment and approach towards both is the same. The focus of medication is to relieve pain, reduce inflammation and maintain or improve joint functioning. There is no specific medical treatment to halt cartilage degeneration. Nor is there any treatment to repair the damaged cartilage. Treatment for osteoarthritis is therefore usually a combination of some medication and a number of conservative, physical treatments such as exercise, weight management, and using supports such as splints, canes, walkers, and braces. Low-impact exercises like swimming, walking and cycling are usually recommended for patients of osteoarthritis.

The main thing to remember especially with secondary osteoarthritis is that it is preventable. A little care and a few lifestyle adjustments can go a long way in slowing down and preventing the onset of osteoarthritis. As with any medical condition, it is best to seek the advice of a professional. And who better to guide you on joint pain than the team at Spinalogy Clinic!

Osteoarthritis: Causes, Risk Factors, and Treatment

How is osteoarthritis diagnosed?

The physician will begin with a complete medical history and a physical examination. During the exam, the doctor will look for an enlarged or bumpy joint, signs of swelling, or decreased range of motion. Your doctor may then order x-rays, which can show a decrease in the cartilage space, new bone formation, or incorrect alignment. In some cases, your doctor may perform an aspiration – the removal of fluid from a swollen joint or bursa – to exclude infection, gout, or rheumatoid arthritis as possible causes of your joint pain.

How is osteoarthritis treated?

There are many treatments for osteoarthritis that are designed to reduce your joint pain, increase mobility, and improve how your joints function.

Non-surgical Interventions:

  • Anti-inflammatory and pain medication, such as acetaminophen and non-steroidal anti-inflammatory drugs
  • Topical analgesics
  • Injections of cortisone to decrease inflammation
  • Injection of viscosupplements (gel-like substances that act like natural joint fluids)
  • Physical therapy
  • Occupational therapy
  • Weight loss
  • Aerobic and strength training exercises
  • Bracing and orthotics
  • Self-management strategies
  • Nutritional supplements

Surgical Interventions:

  • Arthroscopy is a minimally-invasive procedure to diagnose and treat conditions affecting joints. The surgeon first examines the internal structure of the joint through a small video camera inserted through the skin. Additional steps to improve joint function then can be taken, such as the removal of loose cartilage or meniscal repair.
  • Arthroplasty is a surgical procedure to replace or restore a severely osteoarthritic joint to ease pain and improve mobility, thereby adding to the patient’s quality of life.
  • An osteotomy involves the removal of a portion of bone to realign the joint – a temporary treatment for osteoarthritis.
  • Cartilage repair and regeneration can replace damaged cartilage and may be useful for patients with certain types of cartilage defects.

What can I do to prevent osteoarthritis?

Maintaining a healthy lifestyle may help prevent osteoarthritis. Eating nutritious foods, maintaining a healthy weight throughout your life, and exercising regularly to strengthen muscles that protect the joints are three very important methods that may reduce your risk of developing osteoarthritis.

– Chris P.

Osteoarthritis definitions for ICD-10-CM coding

Osteoarthritis definition versus primary osteoarthritis definition versus secondary osteoarthritis definition for ICD-10-CM coding
Osteoarthritis, when not classified as either primary or secondary is the most common type of arthritis which occurs when the protective cartilage on the ends of your bones wears down over time. Arthritis is an inflammation of joint due to infectious, metabolic, or constitutional causes. Osteoarthritis can occur at a higher age and can be more frequent in women. A genetic susceptibility can in addition contribute to the development of osteoarthritis. Osteoarthritis most commonly affects joints in the hands, knees, hips, and spine. The symptoms of osteoarthritis include pain, tenderness, stiffness, loss of flexibility, and grating sensation of a joint. As a sequelae of osteoarthritis, bone spurs may form around the affected joint. Generalized osteoarthritis affecting more than one joint is medically coded as M15.9. Osteoarthritis of the left wrist joint that developed in a 70 year old female patient is medically coded as M19.032.
Primary osteoarthritis is when there is wear-and-tear damage of a specific joint from repetitive use. Primary osteoarthritis can occur as a result of certain occupations. Primary osteoarthritis of the right ankle for a patient that often over-walks for exercise health is medically coded in ICD-10-CM as M19.071 and primary osteoarthritis of the left shoulder for a baseball player is medically coded as M19.012, for example. Secondary osteoarthritis is osteoarthritis secondary to another disease or condition including obesity, repeated trauma or surgery to the joint structures, abnormal joints at birth, gout, rheumatoid arthritis, diabetes, and other hormone disorders. Secondary osteoarthritis from repeated trauma to the right elbow joint is medically coded as M19.221, S59.901D.
Sincerely,
Vino C. Mody Jr., M.D., Lic., Ph.D., COC, CPC, CCS-P, CANPC, CCVTC, 4Med CICP, CNPR, CRMC

About the author

Leave a Reply

Your email address will not be published. Required fields are marked *