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Research Article | Volume 3 Issue 2 (July-Dec, 2022) | Pages 1 - 5
Idiopathic Primary Osteoarthritis of the Knee and Difficulties in Diagnosis
 ,
1
M.B.Ch.B. DM. DRDR, CABM, JBED, Specialist internal medicine and endocrinologist at Al Yarmouk Hospital, Iraq
2
M.B.Ch. B, FICMS Neurology, Specialist internal medicine and neurology at Al Yarmouk Hospital, Iraq
Under a Creative Commons license
Open Access
Received
Aug. 3, 2022
Revised
Sept. 8, 2022
Accepted
Oct. 16, 2022
Published
Nov. 10, 2022
Abstract

50 Patients with presumably primary knee osteoarthritis were evaluated for involvement of other joints. The osteoarthritic group was compared with 50 age matched control group, suffering from low back pain. It was found that 56% of osteoarthritis cases have other joint involvement, compared to 6% of control group if the shoulder joint involvement is excluded (p-value < 0.05). The frequency of joint involvement (articular and or periarticular) in the osteoarthritic group was shoulders (50%), elbows (40%), Wrist (55%), metacarpophalangeal joints (34%), ankles (56%) and metatarsophalangeal joints (34%). On the other side the frequency of joint involvement in the control group (articular and or periarticular) was shoulders (40%), elbows (2%), wrists (6%), metacapophalangeal joints (6%), ankles (16%) and metatarsophalangeal joints (1%). The frequency of symptoms and signs outside the Knee in the Osteoarthritis group can be explained by either an underlying low grade inflammatory joint disease or by a degenerative process which is “Multifocal”. These possibilities will be explained later in the discussion. We conclude that careful clinical and laboratory evaluation, as well as long term follow up is necessary before a firm diagnosis of primary osteoarthritis is to be made. Further studies are needed to uncover the spectrum of what is considered a primary Knee Osteoarthritis and whether many of the causes could be not primary.

Keywords
INTRODUCTION

Osteoarthritis is not a single disease but, it is an end result of primary or secondary joint failure. Inflammatory changes in the synovium are usually minor and secondary [1]. The main signs and symptoms of osteoarthritis are pain which is evoked by use and relieved by rest. Early morning stiffness or after rest is also common but, is usually of less than 30 minutes duration. Mobility limitation is the common end result [1,2]. Primary osteoarthritis is either nodal type, non- nodal or erosive in type [1-3]. The predominantly involved joints are knees, spine, hips, base of the thumb, Distal interphalangeal joints and proximal interphalangeal joints [1-4]. Blood count and systemic inflammatory markers are markers characteristically normal in primary osteoarthritis [4-7]. The radiographic changes offer high specificity. Osteoarthritis is the most common joint disease in humans. By the age of 65 years, 80% have some radiological evidence of osteoarthritis and 30% have symptoms [2]. Osteoarthritis affects both genders, but it is more generalized and severe in older women. Involvement of the metacarpophalangeal joints, wrists, elbows, metatarsophalangeal joints, shoulders and ankles is uncommon in primary Osteoarthritis. In fact, affection of these joints raises the suspicion of diseases other than primary Osteoarthritis [1,3,7]. Similarly elevated systemic inflammatory markers is also in favor of inflammatory joint disease [7-14]. The diagnosis of primary Osteoarthritis may reflect in many cases our inability to discover the primary disorder, which is complicated by osteoarthritis. Studies are needed to explore the real spectrum of the so-called primary Osteoarthritis. The specificity of the diagnostic criteria of primary Knee Osteoarthritis is actually only 69% when the diagnosis is made clinically.

 

Patients and Methods

50 patients whose age is above 50 years, who have unilateral or bilateral knee joint pain of more than two months duration and have radiographic evidence of osteoarthritis were studied as cases of primary knee osteoarthritis according to criteria. Females were 32 patients (64%) and males were 18 patients (36%). Their age range was 51-67 year; the mean age was 56.62+ 5.05. Their mean weight was 77.52+ 7.36 kg [15]. The above group was compared with a control group, which consisted of randomly selected 50 age matched patients complaining of low back pain. Males were 29 patients (58%) and females were 21 patients (42%). Their ages range 51-67 years, the mean age was 54.69 + 3.74. Their mean weight was 73.52+ 4.6.

 

Those patients (sample and control) were studied at the outpatient clinic of Rheumatology and medical rehabilitation department, at Ibin Senna teaching hospital, in Mosul between December 2002 and August 2003.

 

Appropriate history was taken and physical examination was performed for all patients (sample and control) and a project form was filled [16]. The history included details about pain, stiffness, the presence or absence of the systemic manifestation and the presence of other chronic co-morbidity. The examination included the manifestation of joint inflammation, gait, posture and muscle wasting [17].

 

Exclusion Criteria Were Patients With

 

  • Past history of significant joint trauma

  • Past history of fractures or bone infection

  • criteria of chronic inflammatory joint disease

  • systemic metabolic and endocrine disorders

  • History of gout

  • Neuropathic disorders such as diabetes mellitus and tabes dorsalis

  • Bone dysplasia 

MATERIALS AND METHODS

The sphygmomanometer cuff was used for this purpose. The mercury column was fixed at 30 mm Hg. Then the patient was asked to squeeze the rolled cuff, as much as he can. To overcome the problem of dominant hand, both grip forces were recorded and mean value was determined for each patient [18].

 

The systemic inflammatory markers (ESR, CRPC and Latex fixation titer) were recorded for each patient (sample and control). The E.S.R. was considered raised when it was more than (Age+10/2) for females and more than (Age/2) for males [1]. C.R.P and latex fixation for Rheumatoid factor were considered abnormal if they exceeded (6 mg/dl) and (1:40) titer respectively.

 

Empirical scoring was done for the severity of systemic inflammatory marker changes (see below). X-ray of the knee joint was taken for every patient (sample and control). The standing position was chosen. The views were postero-anterior and lateral. The radiological changes were measured, and the measures were utilized in an empirical severity score [19]. In addition, careful attention was given to maintaining consistent imaging parameters to ensure comparability across subjects. All radiographs were assessed by experienced observers to minimize inter-observer variability. These standardized procedures helped strengthen the reliability and accuracy of the severity scoring system [20].

 

Pain Grading

 

  • 0: No Pain.

  • 1: Mild pain that can easily be ignored.

  • 2: Moderate pain that can't be ignored and interferes with the function &needs treatment [22].

  • 3: Sever pain that is present most of the time demanding constant attention.

  • 4: Excruciating totally incapacitating pain.

 

Tenderness Grading

 

  • 0: No tenderness.

  • 1: The patient says that the joint is tender.

  • 2: The patient winces.

  • 3: The patient winces and withdraws the affected part.

  • 4: The patient doesn't allow the joint to be touched.

 

Swelling Grading

 

  • 0: No swelling.

  • 1: Minimal fluid: patellar tap is elicited with difficulty.

  • 2: Mild effusion: patellar tap is easily elicited.

  • 3: Moderate effusion: patellar tap is positive with supra-patellar joint swelling [23].

  • 4: Tense effusion.

 

The Empirical Clinical Severity Scores

 

  • Pain 0-4

  • Tenderness 0-4

  • Knee joint effusion 0-4

  • 1-4-------------mild

  • 5-8------------moderate

  • 9-12---------- severe

 

Empirical Radiological Severity Scores

A. Measurements of radiological changes

 

  • Joint space narrowin

  • Compartmental space narrowing - (1)

  • Diffuse space narrowing. ------- (2)

  • Sub-chondral sclerosis.

  • Compartmental sclerosis. ---------- (1)

  • Diffuse sclerosis. ------------ (2)

  • Sub-chondral cyst formation

  • Small size cyst <2.5 mm ------- (1)

  • Large size cyst >2.5 mm ------- (2)

  • Osteophytes.

  • Large osteophytes----------- (1) according to the radiological reports

  • Small osteophytes. --------- (2) according to the radiological reports 

 

B. Severity scoring of the radiological measurement

1-3----------mild

4-6---------moderate

7-8------------- severe

 

Empirical Systemic Inflammatory Markers Scoring System

A. Criteria for raised systemic inflammatory makers

  • ESR > age+10/2 for females (Elythrocyte Sedimentation Rate.)

  • ESR > age/2 for males……………………. (1)

  • CRPC >6 mg/dl.................................................... (1)

  • Latex Fixation titer >1:40..................................... (1)

 

B. Scoring of the inflammatory markers:

  • Mild: elevation of one marker.

  • Moderate: elevation of any two markers.

  • Severe: elevation of the three markers.

RESULTS

The included 50 patients with knee joint pain (cases) had mean age 56:62+ 5.05 years, range (51-67) Females were 32 patients (64%), and males were 18 patients (36%). Their mean body weight was 77.5+7.32Kg, range (59-101Kg). The mean duration of knee joint pain was (9.3 months) range (2-30 months). On the other hand, the included 50 patients with low back pain (control group) had mean age 52+7.5 years, range (51-67 years); the males were 29 patients (58%) and females were 21 patients (42%). Their mean body weight was 73.52+6.4Kg (56 - 110Kg). The mean duration of low back pain was 4.15 months, range (0.5-7months); demographic feature (Table1).

 

Table 1: Demographic Features of the Study Population

 Var.SampleControl
 GenderNO%Disease Duration (month)Weight (kg)Age (yeas)No.%Disease Duration (month)Weiht (kg) Age (yreas) 
Sex  MeanRangeMeanRangeMeanRange  MeanRangeMeanRangeMeanRange
Female326411.2+320-3075.5+7.360-9556.1+351-6721422.10.5-375.6+5.265-9052+7.551-67
Male18367.7+5.221-2878.1+1.259-10155.3+1.255-6529586.24456877.1+2.175-11056+5.751-66
Total501009.320-3077.5+7.3259-10156.62+5.0551-67501004.150.5-773.52+6.456-11054.69+3.751-67

 

By the use of empirical clinical knee joint severity scoring 21(42%) patients were mildly involved, 28 patients (56%) were moderately involved and only one patient (2%) had severe knee joint involvement, (Tables 2,3,7). 

 

Table 2: The Frequency of Skeletal Involvement (Articular and / or Per Articular) in the Study Population

p valueTotal 50 Patients (controls)Total 50 Patients (cases)Skeletal/ Involvement/ Other than the Knee joint
PercentageNO.%NO.
<0.31540205025Shoulders
<0.001214020Elbows
<0.001635025Wrists
<0.001633417MCP s
<0.0011685628Ankles
<0.001213417MTPs

 

Table 3: Severity Distribution of Skeletal Involvement in the 50 Patients with Knee Osteoarthritis

JointMildModerateSevere
NO.PercentageNO.PercentageNO.Percentage
Knees1122387611
Shoulders153010200.00.0
Elbows20400.00.00.00.0
Wrists16329180.00.0
MCP s9187140.00.0
Ankles173411220.00.0
MTP s1428360.00.0

 

The scoring of systemic inflammatory markers in case group yielded normal readings in 20 patients (40%), mild, moderate and severe readings were 13 patients (26%), 14 patients (28%) and 3 patients (6%) respectively; while in the control group 46 patients (92%) had normal readings, 4 patients had mild readings. Moderate and severe readings did not appear in control group, (Table 4).

 

Table 4: Comparison of Systemic Inflammatory Markers in the Study Population

Systemic Inflammatory MarkersCaseControlX2p–valueOdd Ratio
NO%NOPercentage
Normal2040469230.1250.0180.06
Mild1326485.7410.0174.05
Modern14280016.2790.014-
Severe36003.090.079-
Total501005010032.0070.010-

 

The prolongation of early morning stiffness was significantly marked in the case group, (Table 5).

 

Table 5: Comparison of Early Morning Stiffness Durations in the Study Populations

Early morning Stiffness duration (minutes)CaseControlp–valueOdd Ratio
NOPercentageNOPercentage
Duration > 30 min2244240.0010.016
Duration < 30 min285648960.00210.035
Total50100501000.001-

 

The reading of the grip strength measurement was significantly lower in the case group than in the control group. The age had no any significant statistical effects on early morning stiffness and grip strength measurements, (Table 6).

 

Table 6: Comparison between the Cases and Control Groups in the Duration of Morning Stiffness and the Grip Strength

ParameterCases Mean + SDControls Mean + SDZ-TESTP-Value
Age (years)56.62+5.0554.96+3.771.8610.066
Weight (Kgs)77.52+7.3676.46+11.520.5480.585
Early morning Stiffness (minutes)28.70+12.46.50+6.4111.2430.013
Mean grip strength (mm Hg)149.52+12.32163.76+6.797.1600.021

 

There was significant relation between the duration of early morning stiffness and the degree of severity of knee joint involvement in case group. (Table 7).

 

Table 7: The Relation between the Degree of Knee Joint Severity the Presence of Other Joint Involvement and Early Morning Stiffness

Subgroups According to Severity of

Knee joint involvement

NO. from

Total 50

Patient (cases)

No. from the subgroups with or without other joint involvementParametersEarly morning stiffness Duration in the subgroups of total 50 patientsParametersV
Patients with Other joint involvementPatients Without other Joint involvementDuration of EMS (min)
> 30< 30
NO.%NO.%X2+p - vO - RNO.%NO.%X2+POR
Mild2151016329.380.0010.104112210209.14<0.0010.15
Moderate28234651010.580.0026.72224451010.93<0.0018.2
Severe112000.359--12--N. SN. S-
Total50295821428.959--34681632-N. S-
                    

X2 is used N.S: Non-significant

 

In this study occupation, type of toilet used and the religious habits (kneeling) had no significant statistical effect on the severity of knee joint involvement. According to the empirical radiological scores adopted in this study, 11 patients (22%) of the case group had mild joint involvement, 38 patients (76%) had moderate involvement and only one (2%) had severe involvement.

 

On the other hand, in the control group 22 patients (44%) showed normal radiographic findings and 28 patients (56%) had mild changes; moderate and sever radiographic changes were not detected in the control group, (Table 8(.

 

Table 8: The Deference in Radiographic Severity of the Knee Joint between the Study Populations

Radiographic SeveritCaseControlX2p- valueOdd Ratio
NO%MO%
Normal00224428.2050.0000.0
Mild132628569.3010.012028
Modern26520.00.035.13600.000-
Sever11220.00.012.3600.000-
Total501005010064.4880.000-

 

The skeletal involvement other than knee joint was significantly observed in the case group in comparison to the controls and was related to the degree of knee joint severity.

DISCUSSION

The diagnosis of idiopathic primary osteoarthritis of the knee joints depends on criteria which are according to the (ACR) criteria (86%) specific when both clinical and radiological criteria are used. The specificity will drop to (69%) when only clinical criteria are used [7]. The diagnosis depends on the knee pain as a central core with an age above 50 years, side by side with the stiffness less than half an hour. The Crepitation is also an important factor in favor of the diagnosis of the idiopathic primary osteoarthritis of the knee. The descision of specificity depends on the power to find cases of secondary osteoarthritis at the time of diagnosis or during follow up. The osteoarthritis process is, generally speaking, a slow process which may take years to present clinically, actually (30%) of people over the age of 65 years have symptoms of osteoarthritis while (80%) of them do have radiological osteoarthritis; furthermore, the cause list of secondary osteoarthritis is a long one and it seems that any long-standing joint disorder can lead to secondary osteoarthritis [2]. In this study we found that at least (56%) of the presumably idiopathic primary osteoarthritis of knee (case) have joint manifestation, which are unusual in primary osteoarthritis [4,6,8,13,14,15]. Compared to only (6%) in control group (p value <0.05). Shoulder involvement was excluded from these figures because most cases are thought to be nonarticular, furthermore shoulder involvement was frequent and similar in both groups (cases and controls). The other joints such as metatarsophalangeal joints, wrists elbows, ankles and metatarsophalangeal joints were significantly more symptomatic in the case group. At the same time the same group (cases) may have either reduction in grip strength or prolonged early morning stiffness or systemic inflammatory markers elevation; though the variation in grip strength may be partly related to the predominance of females in the osteoarthritis group [15].

 

These Findings can be explained in Three Ways

 

  • It is possible that the used criteria for primary osteoarthritis lacksspecificity which may allow for the inclusion of a number of low grade chronic inflammatory joint disease [10,21]

  • The other possibility is that once osteoarthritis it established it may lead to secondary systemic inflammatory process involving the joints in a way somehow similar to arthritis following fractures or joint trauma [3]. Another support to this possibility is the episodic inflammatory flares in the so-called erosive or rapidly progressing osteoarthritis

  • It is possible also that idiopathic primary osteoarthritis is frequently not a focal aging process but a systemic degenerative process in the joints, though it is not markedly generalized as in the case of nodal generalized osteoarthritis

CONCLUSION

Whenever diagnoses of “primary, Knee Osteoarthritis is made, the clinician should carefully look for manifestation in other joints and soft tissues. Some cases may turn to be in the category of chronic inflammatory joint disease [15]. Furthermore, whenever inflammatory components are present in the knee or elsewhere, the use of nonsteroidal anti-inflammatory drugs (NSAIDS) should be balanced between its anti-inflammatory benefits and its possible masking effects on the low-grade inflammatory process, which may delay the proper diagnosis [2,12,24].

 

Recommendation

Further studies are needed to explore the role of disease modifying anti-rheumatic agents (DMARDs) in the so, called inflammatory Osteoarthritis [25]. 

REFERENCE
  1. Nuki, G. et al. “Osteoarthritis and related disorders.” Davidson’s Principles and Practice of Medicine, edited by Christopher H. Stell et al., 18th ed., Churchill Livingstone, 1999, pp. 923–1023.

  2. Brandt, Kenneth D. “Osteoarthritis.” Harrison’s Principles of Internal Medicine, edited by S. L. Hauser et al., 15th ed., 2001, pp. 1987–1993.

  3. Moskowitz, Ronald W. “Clinical and laboratory features in osteoarthritis.” Arthritis and Allied Conditions, edited by Daniel J. McCarty and William J. Koopman, 12th ed., Lea & Febiger, 1993, pp. 209–267.

  4. Harris, Edward H., Jr. “Clinical features of rheumatoid arthritis.” Kelly’s Textbook of Rheumatology, edited by Shaun Ruddy et al., 6th ed., W. B. Saunders, 2001, pp. 967–996.

  5. Brandt, Kenneth D. “Management of osteoarthritis.” Kelly’s Textbook of Rheumatology, edited by Shaun Ruddy et al., 6th ed., W. B. Saunders, 2001, pp. 1419–1435.

  6. Salmon, Louis. “Clinical features of osteoarthritis.” Kelly’s Textbook of Rheumatology, edited by Shaun Ruddy et al., 6th ed., W. B. Saunders, 2001, pp. 1409–1412.

  7. Anderson, Ronald J. “Rheumatoid arthritis: Clinical and laboratory features.” Primer on the Rheumatic Diseases, edited by John H. Klippel et al., 12th ed., Arthritis Foundation, 2001, pp. 218–224.

  8. Hochberg, Marc C. “Osteoarthritis: Clinical features.” Primer on the Rheumatic Diseases, edited by John H. Klippel et al., 12th ed., Arthritis Foundation, 2001, pp. 289–292.

  9. Simms, Robert W. “Osteoarthritis.” Cecil Essentials of Medicine, edited by Thomas E. Andreoli et al., 5th ed., W. B. Saunders, 2001, pp. 712–714.

  10. Simms, Robert W. “Nonarticular soft tissue disorders.” Cecil Essentials of Medicine, edited by Thomas E. Andreoli et al., 5th ed., W. B. Saunders, 2001, pp. 715–719.

  11. Howell, David et al. “Etiopathogenesis of osteoarthritis.” Arthritis and Allied Conditions, edited by Daniel J. McCarty and William J. Koopman, 12th ed., Lea & Febiger, 1993, pp. 1735–1765.

  12. Chintzer, Thomas J. “Management of osteoarthritis.” Arthritis and Allied Conditions, edited by Daniel J. McCarty and William J. Koopman, 12th ed., Lea & Febiger, 1993, pp. 1950–1975.

  13. Hough, Aubrey J. “Pathology of osteoarthritis.” Arthritis and Allied Conditions, edited by Daniel J. McCarty and William J. Koopman, 12th ed., Lea & Febiger, 1993, pp. 1700–1716.

  14. Ryan, Laurence M. “Calcium pyrophosphate crystal deposition disease (Pseudogout).” Arthritis and Allied Conditions, edited by Daniel J. McCarty and William J. Koopman, 12th ed., Lea & Febiger, 1993, pp. 1835–1851.

  15. El-Ghoblawy, Hani S. et al.“Evaluating Patients with Arthritis of Recent Onset.” JAMA, vol. 284, 2000, pp. 2368–2373.

  16. Kowanko, I.L. et al. “Domiciliary self-measurement in rheumatoid arthritis and demonstration of circadian rhythmicity.” Annals of the Rheumatic Diseases, vol. 41, 1982, pp. 453–454.

  17. Leach, R.E. et al. “Weight-bearing radiography in osteoarthritis of the knee.” Radiology, vol. 97, 1970, p. 265.

  18. Gardner-Medwin, D. “The clinical examination of the voluntary muscles.” Disorders of the Voluntary Muscle, edited by J. N. Walton, 3rd ed., Churchill Livingstone, 1976, pp. 517–539.

  19. Edwards, R. and M. McDonnell. “Hand-held dynamometer for evaluating voluntary muscle function.” The Lancet, vol. 2, 1975, pp. 757.

  20. Denham, R.A. “Radiological examination of the knee and other special investigations.” Arthritis of the Knee: Clinical Features and Surgical Management, edited by M. A. R. Freeman, Churchill Livingstone, 1980, pp. 101–119.

  21. Beary, John III et al. “Osteoarthritis.” Manual of Rheumatology and Outpatient Orthopedic Disorders, edited by Stephen Paget et al., 4th ed., Lippincott Williams & Wilkins, 2000, pp. 337–348.

  22. Solomon, Louis et al. Apley’s System of Orthopaedics and Fractures. 8th ed., Arnold, 2001, pp. 371–510.

  23. Swash, Michael. Hutchison’s Clinical Methods. 9th ed., Baillière Tindall, 1989, pp. 442.

  24. Furst, Daniel E. and Harold E. Paulus. “Aspirin and other nonsteroidal anti-inflammatory drugs.” Arthritis and Allied Conditions, edited by Daniel J. McCarty and William J. Koopman, 12th ed., Lea & Febiger, 1993, pp. 567–594.

  25. Brandt, Kenneth D. “Second-line drug therapy for osteoarthritis.” Clinical Medicine, vol. 1, 2001, pp. 110–111.

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