Benign Joint Hypermobility Syndrome: Evaluation, Diagnosis, and Management

MAJ Michael R. Simpson, DO, MC, USA

Author Notes
The Journal of the American Osteopathic Association, September 2006, Vol. 106, 531-536.

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Abstract

Benign joint hypermobility syndrome (BJHS) is a connective tissue disorder with

hypermobility in which musculoskeletal symptoms occur in the absence of systemic
rheumatologic disease. Although BJHS has been well recognized in the rheumatology and
orthopedic literature, it has not been discussed in the family medicine literature. Because
most patients with musculoskeletal complaints are first seen by family physicians, it
behooves primary care physicians to be familiar with recognizing and diagnosing BJHS.
When patients with this syndrome are first seen by a physician, their chief complaint is joint
pain, so BJHS can be easily overlooked and not considered in the differential diagnosis. Use
of the Brighton criteria facilitates the diagnosis of BJHS. Treatment modalities include
patient education, activity modification, stretching and strengthening exercises for the
affected joint, and osteopathic manipulative treatment.

Benign joint hypermobility syndrome (BJHS) is the occurrence of musculoskeletal symptoms

in hypermobile individuals in the absence of systemic rheumatologic disease. This syndrome
is thought to be an inherited connective tissue disorder.1,2 The primary clinical manifestations
of BJHS are hypermobility and pain in multiple joints. This syndrome is different from other
disorders that cause local joint hypermobility and generalized joint laxity, such as Marfan
syndrome and Ehlers–Danlos syndrome (EDS).
The Brighton criteria are used to diagnose BJHS, and laboratory tests are used to distinguish
BJHS from other systemic diseases.1,2 Other criteria have been proposed for diagnosis,
including Bulbena's criteria; however, the criteria defined by Brighton are the ones most
frequently cited in the literature.3
Generalized joint laxity is commonly seen in healthy individuals who do not have complaints.
Hypermobility that is not associated with systemic disease occurs in 4% to 13% of the
population.4,5 Hypermobility diminishes as one ages, and it also appears to be related to sex
and race.5 In general, women have greater joint laxity than men, and up to 5% of healthy
women have symptomatic joint hypermobility compared with 0.6% of men.6 People of
African, Asian, and Middle Eastern descent also have increased joint laxity.7–9.
Among studies examining the prevalence of generalized hypermobility in patients referred to
rheumatologists,5,9–11 one study found that hypermobility occurred in 66% of school children
with arthralgia of unknown etiology.10 Another study showed a similar prevalence of
hypermobility in children; however, there was no association between hypermobility and the
development of arthralgia.11 These data suggest that generalized hypermobility exists without
joint pain and it does not necessarily lead to arthralgia. Furthermore, patients with
hypermobility often lead normal lives and do not have BJHS or another connective tissue
disorder.
Hypermobility may occur in several different connective tissue disorders including Marfan
syndrome, EDS, and osteogenesis imperfecta. It may also be found in chromosomal and
genetic disorders such as Down syndrome and in metabolic disorders such as homocystinuria
and hyperlysinemia. Recurrent dislocation of the shoulder and patella as well as other
orthopedic abnormalities are associated with joint laxity. Juvenile rheumatoid arthritis may
also be associated with hypermobility, but many times, systemic symptoms are involved.7
Patients with BJHS have generalized hypermobility as well as chronic joint pain and other
neuromusculoskeletal signs related to a defect in collagen.7–9
Benign joint hypermobility syndrome has a strong genetic component with an autosomal
dominant pattern. First–degree relatives with the disorder can be identified in as many as
50% of cases. The syndrome appears to be due to an abnormality in collagen or the ratio of
collagen subtypes. Mutations in the fibrillin gene have also been identified in families with
BJHS.12
So, why do patients with BJHS present mainly with joint pain? It is thought that excessive
joint laxity leads to wear and tear on joint surfaces and strains or fatigues the soft tissue
surrounding these joints. Some studies also suggest that proprioception in the joints of
patients with BJHS is impaired. This impairment can also lead to excessive joint trauma due
to impaired sensory feedback from the joint affected.1–4
Figure 1.
Questions physicians should ask patients to detect benign joint hypermobility syndrome.
(Reproduced with permission from Hakim AJ, Cherkas LF, Grahame R, Spector TD,
MacGregor AJ. The genetic epidemiology of joint hypermobility: A population study of
female twins. Arthritis Rheum. 2004;50:2640–2644.)

View Original | Slide (.ppt)

Review of the Literature
A search for the terms hypermobility, hypermobility syndrome, joint hypermobility, and
benign joint hypermobility syndrome on MED-LINE and the MD Consult Core Collection
covering 1966 through 2005 yielded 263 reports on BJHS looking at history, clinical
presentation, diagnosis, treatment, and prognosis. Surveyed articles include review articles
and case-control, retrospective, and observational studies, but no randomized controlled
trials. In addition, the role of osteopathic manipulative treatment (OMT) of patients for
hypermobility and chronic pain was researched by using the same databases with the key
words manipulation and osteopathic manipulation used separately with hypermobility.
Twenty articles were found on manipulation and hypermobility; however, none of these
articles specifically address osteopathic manipulation.
Clinical Presentation
The signs and symptoms of BJHS are variable. Most commonly, the initial complaint in a
hypermobile patient is joint pain, which may affect one or multiple joints and may be
generalized or symmetric. Primary care physicians can use the five simple questions (Figure
1) to aid in recognizing hypermobility.13 The onset of symptoms can occur at any age, and
many patients have been referred to specialists in orthopedics, rheumatology, or physiatry.
Typically, children have self-limited pain in multiple joints; however, pain can last for a
prolonged time and may become constant in adulthood. Pain may involve any joint but most
commonly involves the knee and ankle, presumably because they are weight–bearing joints.
Physical activity or repetitive use of the affected joint often exacerbates the pain.
Consequently, pain usually occurs later in the day and morning stiffness is uncommon. Less
common symptoms are joint stiffness, myalgia, muscle cramps, and nonarticular limb pain.
Patients with BJHS often say that they are “double-jointed” or that they can contort their
bodies into strange shapes (ie, volitionary subluxation) or do the splits. Such an admission,
however, is not necessary for including BJHS in the differential diagnosis. Patients with
BJHS may also have a history of shoulder or patellar dislocation.
Patients with BJHS may have a family history of “double-jointedness” or recurrent
dislocations. Other presentations include easy bruising, ligament or tendon rupture,
congenital hip dysplasia, and temporomandibular joint dysfunction.1,7,14
Findings of the physical examination vary based on the joint saffected. Pain in response to
manipulation of the joint is common. Mild effusions are not common but may be present.
Clinically significant tenderness along with redness, swelling, fever, or warmth suggests
inflammation and is not present in patients with BJHS.4,7
Signs of a typical connective tissue disorder may be present, including scoliosis, pes planus,
genu valgum, lordosis, patellar subluxation or dislocation, marfanoid habitus, varicose veins,
rectal or uterine prolapse, and thin skin (Figure 2). The association of BJHS with mitral valve
prolapse (MVP) is a subject of controversy. Early studies showed an association between
MVP and BJHS,15 but later studies have questioned this association because of stricter
echocardiographic criteria for MVP.17 Primary care physicians should refer patients with
hypermobility in whom cardiac findings suggest MVP to a cardiologist for further evaluation
to rule out more serious cardiac abnormalities and connective tissue disorders.7,15–17
Diagnosis
Determining the Beighton score (Figure 3) is essential for making the diagnosis. The first
step is to calculate the Beighton score, which is a measure of generalized joint laxity.1
Physicians calculate this score by doing five simple maneuvers (Figure 4) that can be
completed in 45 to 60 seconds. A Beighton score of 4 or more points is considered indicative
of generalized joint laxity. Most patients with BJHS have symmetric joint laxity. The
Brighton criteria were developed to establish diagnostic criteria for BJHS. Using these
criteria helps physicians to distinguish BJHS from other connective tissue disorders.1,4,14
Diagnosis of BJHS is one of exclusion. For patients with painful or swollen joints, it is
important to rule out inflammatory, infectious, and autoimmune causes. Workup may include
a complete blood cell count, erythrocyte sedimentation rate, rheumatoid factor, antinuclear
antibody test, serum complement (C3, C4, CH50) levels, and serum immunoglobulin (IgG,
IgM, IgA) levels. Any of these test results that are not within the normal reference range
suggest an alternate diagnosis. Sometimes, patients with BJHS have an effusion, but the joint
aspirate shows a noninflammatory pattern from meniscal and cartilage irritation.
Figure 2.
Neuromusculoskeletal signs and potential sequelae from benign joint hypermobility
syndrome.

View Original | Slide (.ppt)

Benign joint hypermobility syndrome needs to be distinguished from other disorders that
share many common features, such as Marfan syndrome, EDS, and osteogenesis imperfecta.
Generalized hypermobility is a common feature in all these hereditary connective tissue
disorders and many features overlap, but often distinguishing features are present that enable
differentiating these disorders.
Figure 3.
Brighton criteria, based on determination of the Beighton score ( Figure 4 ), is used to make
the diagnosis of benign joint hypermobility syndrome. (Note: Readers should not be confused
by the similarity of these two names. “Beighton” is the correct spelling of the name of the
score, and “Brighton,” the correct spelling of the name of the criteria.)

View Original | Slide (.ppt)

Ehlers–Danlos Syndrome
Ehlers–Danlos syndrome comprises a group of connective tissue disorders that have gross
joint laxity and may have purple papyraceous scars, skin hyperelasticity, and skin fragility
that leads to easy bruising. Similarly to BJHS, EDS is inherited in an autosomal dominant
fashion and is due to a defect in collagen. Of the many different types of EDS that exist, the
most common are types I, II, and III. Benign joint hypermobility syndrome is thought to be a
mild variation of EDS and most closely resembles EDS type III (hypermoblity type), which
consists of joint pain, marked hypermobility, mild extra-articular involvement, and mild skin
changes without scarring.18,19 Researchers have suggested that BJHS lies on a continuum
with EDS and may be its mildest form because of their overlapping features.7,18

View Original | Slide (.ppt)

Marfan Syndrome
Patients with Marfan syndrome often have a family history of the syndrome and tend to have
cardiac and ocular features. Marfan syndrome is an autosomal dominant disorder in patients
with a tall, thin body habitus (marfanoid habitus), generalized joint hypermobility, elongated
fingers (arachnodactyly), myopia, and lens dislocation. Osteogenesis imperfecta is also
characterized by a defect in collagen. Patients have excessive joint laxity, thin blue sclera,
and bone fragility leading to multiple fractures and bony deformities.
Juvenile Rheumatoid Arthritis
Juvenile rheumatoid arthritis may be considered in children with hypermobility and joint
pain, but its diagnosis requires the onset of arthritis before the age of 16 years, inflammation
of one or more joints, and the exclusion of other rheumatic disorders.
Management
The first step in managing BJHS is to emphasize to patients that this syndrome is a
nonprogressive, noninflammatory connective tissue disorder.1,10,14 Effective treatment may be
accomplished with lifestyle modification, altering the patient's exercise regimen, joint
protection, and proper body mechanics.
For acute symptoms, nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen have
often been used for pain control. Joint complaints in these patients are not thought to be due
to inflammation, so the use of NSAIDs for anything other than pain is disputed.7,8,14 For
moderate or severe pain, rest and abstaining from aggravating activities may improve
symptoms. Physical therapy and joint protection may also help.8,14
Long-term management of BJHS typically focuses on modification of activities, especially if
they induce symptoms. Excessive joint movement is associated with the development of
symptoms in patients with BJHS. Often, vigorous and repetitive activities have been targeted
as aggravating factors. Overtraining, poor pacing, too many performances or athletic
competitions, and focusing on joint flexibility rather than stability may all increase joint pain
and the risk of injury.20 If avoidance of these activities is not an acceptable option for
patients, physicians may try other approaches. NSAIDs taken before competition often may
reduce symptoms. Also, starting a strengthening program to provide muscular stability and
stabilization to the joint may be beneficial. Stretching techniques that are targeted to isolate
tight muscles without stressing the surrounding joints may reduce symptoms by improving
balance and control.14
Strength training should consist of a combination of both open kinetic (distal extremity
moves freely) and closed kinetic chain (distal extremity meets resistance) exercises. Closed
kinetic chain exercises often simulate functional demands of an extremity, while open kinetic
chain activities are better for more targeted strength training.14
Focusing on improving the proprioception of a joint may improve symptoms (eg, using a
wobble board).21,22 Sometimes, supportive splints along with appropriate footwear protect the
joint, and supportive joint taping improves joint proprioception.21 Focused exercises to
improve muscle strength, balance, and coordination may help improve joint stability and
proprioception. Improvement of proprioception may reduce strain to the ligaments
surrounding the joint and avoid further injury.21,22
Along with exercise therapy, OMT is a useful adjunctive treatment modality for BJHS.
Thrust treatment techniques applying high velocity/low amplitude forces are the most widely
used, but because of the increased tissue fragility seen in BJHS and weak supporting
structures of the joint, gentler techniques like facilitated positional release and counterstrain
are good alternatives. Osteopathic manipulative treatment helps induce articular release
resulting in increased joint motion, and reduced pain as well as improved blood flow,
lymphatic drainage, and proprioception.15 It is thought that OMT can lead to hypermobility;
however, not enough research has been conducted to confirm this hypothesis, and it is
currently recommended that OMT be limited to no more than three times per week.23 To help
patients return to their activities while decreasing their symptoms and joint stress, osteopathic
physicians should consider all these factors.24,25
Prognosis
The prognosis for patients with BJHS is generally good owing to the syndrome's
nonprogressive nature and decreased joint laxity and symptoms that occur with age.
However, patients need to be aware of the potential sequelae that have an increased
frequency associated with BJHS. These sequelae include acute ligament and soft tissue
injury, overuse injury, joint instability, possible increase in fractures and scoliosis, and
increased frequency of uterine and rectal prolapse. In addition, these patients may be
predisposed to osteoarthritis from years of excessive joint motion.8 Also, an association
between BJHS and panic disorder has been shown.26 Despite these sequelae, patients should
remain as active as possible. Altering their exercise regimen may avoid chronic joint pain.
Good training strategies include slow, disciplined training, correct biomechanics, and
effective proprioception.20
Given the many sequelae that may develop and the potential impact of BJHS on quality of
life, some experts are questioning why BJHS is called a “benign” disorder; instead, they refer
to the disorder as “joint hypermobility syndrome.”18 However, most rheumatologists still
refer to it as BJHS. In the future, more rheumatologists may use the changed name—joint
hypermobility syndrome—because of the disorder's potential effects on quality of life.
The potential complications of BJHS underscore the importance of making an early diagnosis
and educating the patient.
Comment
Osteopathic physicians predominantly practice primary care medicine, and most patients with
musculoskeletal complaints first see a primary care physician and are then referred to a
rheumatologist. Hypermobility is a common cause of unexplained joint pain, yet it is often
misdiagnosed in primary care. According to one source, primary care providers recognized
generalized hypermobility in less than 10% of patients with generalized hypermobility who
were referred to rheumatologists.18 Therefore, physicians need to be aware of the clinical
presentation of BJHS to enhance their diagnostic acumen.
Benign joint hypermobility syndrome is the presence of musculoskeletal complaints in
hypermobile individuals in the absence of systemic rheumatologic disease. It is a connective
tissue disorder with a defect in collagen. The Brighton criteria are used to make the diagnosis.
Education, activity modification, and exercise therapy to improve muscular stability and
proprioception at specific joints are essential to symptom management. And, OMT is a useful
adjunctive treatment modality to help reduce pain and improve proprioception.
Finally, primary care physicians are the best resource to educate patients with BJHS about
their illness, potential complications, and prognosis. Furthermore, a prompt diagnosis
improves pain control and decreases disruptions in these patients' physical activities, school,
work, and quality of life.18 Thus, by being the first medical contact for most of their patients
with BJHS, physicians in primary care have the opportunity to diagnose and address BJHS
and reduce the incidence of potential long-term sequelae, chronic pain, and traumatic
injuries.
This paper has been reviewed by the US Army, and the content of the manuscript does not
necessarily reflect the views of the US Army or the Department of Defense.

1
Grahame R. The revised (Brighton 1998) criteria for the diagnosis of benign joint
hypermobility syndrome (BJHS). J Rheumatol. 2000;27:1777 –1779.
2
Hakim AJ, Cherkas LF, Grahame R, Spector TD, MacGregor AJ. The genetic epidemiology
of joint hypermobility: a population study of female twins. Arthritis Rheum. 2004;50:2640–
2644. Available at: http://www3.interscience.wiley.com/cgi-
bin/fulltext/109581945/HTMLSTART. Accessed August 29, 2006.
3
Bulbena A, Duro JC, Porta M, Faus S, Vallescar R, Martin–Santos R. Clinical assessment of
hypermobility of joints: assembling criteria. J Rheumatol. 1992;19:115 –122.
4
Biro F, Gewanter HL, Baum J. The hypermobility syndrome. Pediatrics. 1983;72:701 –706.
5
Seckin U, Sonel Tur B, Yilmaz O, Yagci I, Bodur H, Arasil T. The prevalence of joint
hypermobility among high school students. Rheumatol Int. 2005;25:260 –263.
6
Engelbert R, Uiterwaal C, Van de Putte E, Helders P, Sakkers R, Van Tintelen P, et al.
Pediatric generalized joint hypomobility and musculoskeletal complaints: a new entity?
Clinical, biochemical, and osseal characteristics. Pediatrics. 2004;113:714–719. Available at:
http://pediatrics.aappublications.org/cgi/content/full/113/4/714. Accessed August 29, 2006.
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Everman DB, Robin NH. Hypermobility syndrome. Pediatr Rev. 1998; 19:111 –117.
8
Finsterbush A, Pogrund H. The hypermobility syndrome. Clin Orthop Relat Res. May(1982).
: 124–127.
9
Larsson LG, Baum J, Mudholkar GS, Kollia GD. Benefits and disadvantages of joint
hypermobility among musicians. N Engl J Med. 1993;329:1079–1082. Available at:
http://content.nejm.org/cgi/content/full/329/15/1079. Accessed August 29, 2006.
10
Gedalia A, Brewer EJ. Joint hypermobility in pediatric practice–a review. J Rheumatol.
1993;20:371 –374.
11
de Inocencio Arocena J, Ocaña Casas I, Benito Ortiz LB. Laxitud articular: prevalencia y
relación con dolor musculosquelético. [Joint hypermobility: prevalence and relationship with
musculoskeletal pain.] An Pediatr (Barc). 2004;61:162–166. Available at:
http://db.doyma.es/cgi-
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ag=162. Accessed August 29, 2006.
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Magnusson SP. Viscoelastic properties and flexibility of the human muscle–tendon unit in
benign joint hypermobility syndrome. J Rheumatol. 2001;28:2720 –2725.
13
Hakim AJ, Grahame R. A simple questionnaire to detect hypermobility: an adjunct to the
assessment of patients with diffuse musculoskeletal pain. Int J Clin Pract. 2003;57:163 –166.
14
Russek LN. Examination and treatment of a patient with hypermobility syndrome. Phys Ther.
2000;80:386–398. Available at: http://www.ptjournal.org/cgi/content/full/80/4/386. Accessed
August 29, 2006.
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Grahame R, Edwards JC, Pitcher D, Gabell A, Harvey W. A clinical and echocardiographic
study of patients with the hypermobility syndrome. Ann Rheum Dis. 1981;40:541 –546.
16
Bird HA, Barton L. Joint hyperlaxity and its long-term effects on joints. J R Soc Health.
1993;113:327 –329.
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Mishra MB, Ryan P, Atkinson P, Taylor H, Bell J, Calver D, et al. Extra-articular features of
benign joint hypermobility syndrome. Br J Rheumatol. 1996;35:861 –866.
18
Adib N, Davies K, Grahame R, Woo P, Murray KJ. Joint hypermobility syndrome in
childhood. A not so benign multisystem disorder? Rheumatology (Oxford). 2005;44:744 –
750.
19
Skoumal M, Haberhauer G, Mayr H. Begleiterkrankungen bei primarer gelenkhypermobilitat.
Med Klin. 2004;99:585 –590.
20
McCormack M, Briggs J, Hakim A, Grahame R. Joint laxity and the benign joint
hypermobility syndrome in student and professional ballet dancers. J Rheumatol.
2004;31:173 –178.
21
Perlau R, Frank C, Fick G. The effect of elastic bandages on human knee proprioception in
the uninjured population. Am J Sports Med. 1995;23:251 –255.
22
Hall MG, Ferrell WR, Sturrock RD, Hamblen DL, Baxendale RH. The effect of
hypermobility syndrome on knee joint proprioception. Br J Rheumatol. 1995;34:121 –125.
23
Protapapas MG, Cymet TC. Joint cracking and popping: understanding noises that
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Advertisement

RECURRENT SHOULDER
DISLOCATIONS AND HYPERLAXITY
1. Akhtar M.A. and
2. Robinson C.M.

+ Author Affiliations

1. Edinburgh, UK

1. M A Akhtar, 72 Whitacres Road, Glasgow G53 7LJ, UK

m_adeel_akhtar@yahoo.com

Abstract
This study was performed to assess the incidence of generalised ligament laxity in patients
presented with recurrent shoulder dislocations.

Prospective data was collected for 38 patients with recurrent shoulder dislocations and 43
patients with clavicle fractures as a control group between May 2007 and July 2009,
including demographic details, mechanism of injury, number of dislocations and hyperlaxity.
Clinical examination was used to assess the ligament laxity using the Beighton score.

The mean age was 29 years with a range from 14-40 years. There were 36 males and 2
females. The left shoulder was involved in 21 patients; right in 13 patients and 4 patients had
bilateral shoulder dislocations. The average number of dislocations was 3 with a range from
2-17, while the average number of subluxations was 4.5 with a range from 0-35. The average
Beighton score for the patients with recurrent shoulder dislocations was 2.8 with a range from
0-8. 17 patients (45%) in this group had a Beighton score of 4 or more as compared to the
control group that had only 12 patients (27%) There was a statistically significant difference
between the 2 groups with a P value of < 0.05. 8 patients (21%) fulfilled the Brighton criteria
for BJHS. The most common cause of recurrent shoulder dislocation was sports related
injuries in 26 patients (68%). The most common sport was football in 14 patients (37%)
followed by rugby in 10 (26%) patients.

We looked at the incidence of generalised ligament laxity in patients with recurrent shoulder
dislocations and found a statistically significant difference as compared with the control
group. 21% of the patients fulfilled the Brighton criteria for BJHS but 45% had a Beighton
score of 4 or more. Appropriate advice should be given to these patients with hyperlaxity and
the timing of shoulder stabilisation should be carefully decided.

 General

 Copyright © 2010, British Editorial Society of Bone & Joint Surgery

Lax Ligaments – Causes, Symptoms, and

Treatment

Authored by
Dr. Gregg Congdon

Reviewed by
Dr. Donald Pelto

Lax ligaments, or ligament laxity, may occur anywhere in the body and can be a major cause
of chronic pain. Loose ligaments — a condition sometimes referred to as being “double
jointed” — may be confined to the feet, but more often the condition is present in all joints.

When this condition affects joints over the entire body, it is called generalized joint
hypermobility. Young people with this condition may lose some of their hyper-laxity as they
age, but people over the age of 40 often have recurrent joint problems and almost always
have chronic pain.

Joint hypermobility is also a common feature of chronic fatigue syndrome.

Why Do I Have Lax Ligaments?
Ligament laxity may be genetic and affect an individual from a very early age. Joint
hypermobility may be a feature of several genetic disorders, including Marfan syndrome,
Ehlers-Danlos syndrome, and Down’s syndrome.

Joint injuries often damage ligaments as well, either by stretching them abnormally or by
tearing them.

An injured ligament that does not heal properly, even after the application of RICE (Rest, Ice,
Compression, and Elevation), may be loose or lax. Lax ligaments are not capable of
supporting joints as effectively as healthy ones.

Thus, affected persons may be prone to further injury, and may compensate for the weakness
by overusing other parts of their bodies.

Lax Ligaments Symptoms To Look For

People with extremely lax (or hypermobile) joints can bend their elbows or knees past a
position of neutrality. They can also easily place their hands flat on the floor while bending
forward from the waist. The ability to touch the thumb to the forearm is also common.

People with lax ligaments may not have any pain or other symptom, but foot and ankle
problems may develop as a result of lax ligaments, and these conditions can cause pain. Such
conditions include:

 Flexible flatfoot: This is caused by lax ligaments in the foot, resulting in a flattened
arch. The bones and joints in the arch of the foot are otherwise normal. Flexible flat
feet are normal in all children under the age of three. After that age, children usually
outgrow flexible flatfoot as their foot ligaments develop. Ligaments that remain lax
into later childhood are usually not painful. Although some affected children may
report pain after playing sports, most will be able to function normally. The
 development of future foot problems, such as arthritis, tendonitis, and deformities, is
unlikely in children with flexible flat feet.
 Ankle sprains: Ankle sprains may be caused by awkward foot placement, irregular
surfaces, weak muscles, or wearing shoes with spiked heels. You may be more likely
to sprain an ankle if your ligaments are loose. The symptoms of a sprained ankle
usually follow trauma. You may have severe pain and not be able to put any weight
on your foot, or you may walk with a limp. Sometimes the foot becomes swollen, red,
or bruised.
 Osteoarthritis: Extreme hypermobility may decrease one’s ability to sense joint
position. This can contribute to joint damage and ultimately lead to degenerative joint
conditions, such as osteoarthritis. A similar scenario can occur in people with severe
ligament injury. The injured ligament may tighten up or be permanently stretched,
leaving some degree of laxity or looseness in the adjacent joint. The residual laxity
creates a sense of instability during activity, which can result in further injury or a
predisposition to premature arthritis in the involved joint.

How Are Lax Ligaments Diagnosed?

Your doctor will assess ligament/joint laxity by measuring range of motion. A simple test for
loose ligaments is to see how far your index finger bends backwards. If you can bend it
backward 90 degrees without discomfort, you have loose ligaments.

Your doctor may use a tool called the Beighton score. One point is assigned for each elbow
and knee that can extend more than 10 degrees, for each thumb that can be apposed to the
flexor surface of the forearm, and for each fifth finger that can be bent backward more than
90 degrees; one point is also assigned for placing the palms on the floor with the knees
straight.

A score of 5 or more is considered positive, but you may still have joint laxity if the test is
negative.

Your doctor will also look for signs of connective tissue disorders and joint hypermobility
syndromes—for instance, people with Ehlers-Danlos syndrome often have skin elasticity.

If your doctor suspects one of these conditions, you may be referred for further evaluation
with an echocardiogram, ophthalmologic examination, or other type of testing.

How Are Lax Ligaments Treated?

Because lax ligaments themselves often do not cause pain, they generally do not require
treatment.

However, if you have musculoskeletal problems caused by lax ligaments or hypermobility,

your doctor will probably suggest conventional medical treatments, which include
physiotherapy and pain medicines. Strength training of muscles may also be recommended.

People who suffer from hereditary joint laxity are advised to avoid joint hyperextension,
impact activity, and resistance exercise to minimize the risk of subluxation and dislocation.
Myofascial release (with heat, massage, or other means) may provide some pain relief. A
lifelong program of low-resistance muscle toning, gradually increasing repetitions and
frequency of exercise, helps stabilize loose joints and may minimize future pain and/or delay
the onset of arthritis.

Surgical intervention to improve joint stability often fails or provides only temporary benefit.

Flexible flatfoot is not a benign condition, and it often results in osteoarthritis and long-term
disability.

Orthotic therapy can help stabilize the foot and ankle to reduce injuries and prevent
irreversible damage to joints. Heel cord stretching can reduce any tightness in the calf and
lower limb muscles.

If you have painful flexible flatfoot, your doctor will first determine the anatomical cause of
the pain. In some cases, surgery may be indicated, but it is not recommended in patients with
joint hypermobility, such as those with Marfan syndrome, Ehlers-Danlos syndrome, or
Down’s syndrome.

For an ankle sprain or ligament injury, early treatment involves RICE to prevent and resolve
any associated swelling.

When the swelling and pain have subsided, further examination will reveal which ligaments
are affected and how severe the injury is. Surgical repair of lax ligaments will generally be
considered, although in most cases conservative measures are attempted first.

http://www.footvitals.com/ligaments/lax-ligaments.html

Phys Ther. 2008 Dec; 88(12): 1506–1516.

doi: 10.2522/ptj.20060223

PMCID: PMC2599794

Instability, Laxity, and Physical Function in

Patients With Medial Knee Osteoarthritis
Laura C Schmitt, G Kelley Fitzgerald, Andrew S Reisman, Katherine S Rudolph

Author information ► Article notes ► Copyright and License information ►

This article has been cited by other articles in PMC.

Go to:

Abstract
Background and Purpose: Studies have identified factors that contribute to functional
limitations in people with knee osteoarthritis (OA), including quadriceps femoris muscle
weakness, joint laxity, and reports of knee instability. However, little is known about the
relationship among these factors or their relative influence on function. The purpose of this
study was to investigate self-reported knee instability and its relationships with knee laxity
and function in people with medial knee osteoarthritis (OA).

Participants: Fifty-two individuals with medial knee OA participated in the study.

Methods: Each participant was classified into 1 of 3 groups based on reports of knee
instability. Limb alignment, knee laxity, and quadriceps femoris muscle strength (force-
generating capacity) were assessed. Function was measured with the Knee Injury and
Osteoarthritis Outcome Score (KOOS) and a stair-climbing test (SCT). Group differences
were detected with one-way analyses of variance, and relationships among variables were
assessed with the Eta2 statistic and hierarchical regression analysis.

Results: There were no differences in alignment, laxity, or strength among the 3 groups.
Self-reported knee instability did not correlate with medial laxity, limb alignment, or
quadriceps femoris muscle strength. Individuals reporting worse knee instability scored
worse on all subsets of the KOOS. Self-reported knee instability scores significantly
contributed to the prediction of all measures of function above that explained by quadriceps
femoris muscle force, knee laxity, and alignment. Neither laxity nor alignment contributed to
any measure of function.

Discussion and Conclusion: Self-reported knee instability is a factor that is not directly
associated with knee laxity and contributes to worse function. Further research is necessary to
delineate the factors that contribute to self-reported knee instability and reduced function in
this population.

Tibiofemoral joint osteoarthritis (OA) is one of the most common and disabling medical
conditions in the United States and worldwide.1–7 Knee OA is responsible for more chronic
disability than any other medical condition and is one of the most frequent medical
problems.2,3,8 Within the knee joint, the medial compartment is the most often involved.9,10

Studies8,11,12 have identified factors that contribute to disability and functional limitations in
people with knee OA, and one of the most notable factors is decreased quadriceps femoris
muscle strength (force-generating capacity). Quadriceps femoris muscle weakness is not only
associated with diminished function8,11 but is also an important predictor of functional
decline.13 Quadriceps femoris muscle strength training, therefore, is typically recommended
for people with knee OA. However, recent work indicates that the relationship between
quadriceps femoris muscle strength and physical function is not as strong in people with
excessive frontal-plane knee laxity,14 a common characteristic in people with knee OA.15,16
Furthermore, the combination of strong quadriceps femoris muscles and excessive
mediolateral knee laxity is associated with higher rates of OA progression.17 This suggests
that rehabilitation interventions that focus on quadriceps femoris muscle strengthening alone
may not be the most effective for all people with knee OA.

Much attention has been paid to joint laxity in people with knee OA due to its prevalence in
this population15,16 and its reported relationship with functional limitations.14 Joint laxity is a
clinical sign that is measured passively; however, it is presumed that excessive passive
motion in the knee joint automatically leads to instability during dynamic and functional
activities. Studies have shown that some individuals with increased anterior knee laxity due
to anterior cruciate ligament (ACL) deficiency report no symptoms of knee instability18–21
and use different neuromuscular activation strategies compared with the strategies used by
people who do report knee instability.22–25 Therefore, neuromuscular control strategies appear
to play a role in stabilizing the knee even in the face of impaired passive restraints.

Recent work26–28 has suggested that self-reported knee instability (the sensation of shifting,
buckling, or giving way of the knee) negatively affects the function of people with knee OA.
Fitzgerald et al27 showed that a substantial number of people with knee OA report sensations
of knee instability during daily activities. Furthermore, they found that self-reported knee
instability significantly lowers physical function beyond the influence of pain, reduced knee
range of motion, and quadriceps femoris muscle weakness.27 Other common characteristics
of people with knee OA that have been associated with worse function, such as knee
laxity14,29 and knee alignment,14,29 were not evaluated by Fitzgerald et al.27 The relationships
among these factors with self-reported knee instability and their influences on function need
to be delineated.

The relationship between medial knee laxity and self-reported knee instability in people with
medial knee OA is unclear. If medial knee laxity and self-reported knee instability influence
daily function independently, treatment plans should address both conditions. If, as current
literature24 suggests, self-reported knee instability has a greater influence on function than
laxity, then addressing self-reported knee instability should be the focus of rehabilitation.
Therefore, in people with medial knee OA, the aims of this work were: (1) to investigate the
relationship between self-reported knee instability and medial knee laxity, varus alignment,
and quadriceps femoris muscle force; (2) to compare the level of function of participants
classified by reports of knee instability; and (3) to investigate the influences of self-reported
knee instability, medial laxity, varus alignment, and quadriceps femoris muscle force on
function.

Go to:

Method
Participants

Individuals with diagnosed medial knee OA were referred from local physicians and were
recruited from the community. Participants were included if they had grade II or greater
Kellgren and Lawrence (K-L) radiographic changes30 in the medial tibiofemoral
compartment, with grades 0 or I in the lateral tibiofemoral and patellofemoral compartments.
Radiographic changes were determined from standing bent posterior-anterior view, lateral
view, and sunrise view radiographs. If a potential participant had bilateral knee OA that fit
the criteria, the more symptomatic knee was identified by the individual and used in the
analysis. Participants were excluded if they had a history of other orthopedic injuries in the
lower extremities (eg, knee ligament injuries) or spine, used an assistive device, had a history
of neurologic injury, had a history of rheumatoid arthritis, were pregnant, or had undergone a
joint replacement or skeletal realignment procedure in either lower extremity. All participants
signed an informed consent statement approved by the Institutional Review Board of the
University of Delaware.

Participants were classified into groups based on their reports of knee instability. Knee
instability was measured using the Knee Outcome Survey–Activities of Daily Living Scale31
(KOS-ADLS), which is a self-report measure of function. One question from the KOS-ADLS
relating to functional stability of the knee (IKOS) was used to classify participants as having
stable or unstable knees. The IKOS has been shown to be a reliable measure of self-reported
knee instability in patients with knee OA.27 Participants rated the severity of knee instability
on a 6-point scale in response to the question, “To what degree does giving way, buckling, or
shifting of your knee affect your level of daily activity?” Definitions of the scores are shown
in Table 1. Participants were classified into 1 of 3 self-reported knee instability groups: those
with no knee instability (I0 group) (IKOS score=5), those with mild knee instability that does
not affect function (Im group) (IKOS score=4), or those with knee instability that affects
function (If group) (IKOS score ≤3) (Tab. 1).

Table 1.

Self-report Measure of Knee Instability (IKOS) From Knee Outcome Survey–Activities of Daily Living31
and Frequency of Responses

The sample size estimate for detecting differences in function between participants with
stable knees and those with unstable knees was based on a large effect size, which was found
in a previous study in our laboratory of people with medial knee OA.32 A difference in
function scores between participants with self-reported knee instability and those without
self-reported knee instability was 18, which is reported to reflect clinically meaningful
changes in function for people with knee OA.33 Based on variability measures from the pilot
work, a difference in population means of 18, and an alpha level of .05, a sample size of 12
participants per group was required to achieve 1–β=0.80.

A total of 52 participants were enrolled, with at least 12 participants in each self-reported

knee instability group. Group characteristics are shown in Table 2. All data were collected
over 2 testing sessions. During the first session, self-assessment questionnaires were
completed, physical function was assessed, and quadriceps femoris muscle strength was
evaluated. During the second session, radiographic assessments of tibiofemoral joint
alignment and frontal-plane laxity were completed.

Table 2.

Group Characteristicsa
Self-assessment of Function

The Knee Injury and Osteoarthritis Outcome Score34,35 (KOOS) was used as a self-report
measure of function. The KOOS covers 5 separate dimensions of knee function: Pain,
Symptoms, Activities of Daily Living (ADL), Sport and Recreation Function (Sport), and
Knee-Related Quality of Life (QOL). Each dimension, or subset, is scored separately and
evaluated independently. The KOOS includes questions from the Western Ontario and
McMaster Universities Osteoarthritis Index (WOMAC) and has been shown to be a valid,
reliable, and responsive measure of overall knee joint function in people with OA.36 On the
KOOS, all dimensions are scored from 0 to 4, and then scores are transformed to a percentage
score of 0 to 100, with 0 representing extreme knee problems and 100 representing no knee
problems.34

Performance-Based Assessment of Physical Function

A timed stair-climbing test (SCT) was used as a performance-based measure of function.

Participants were timed with a stopwatch as they ascended and descended a set of 12 stairs
(18 cm high). The participants were instructed to perform the task as quickly as they felt safe
and comfortable. They were encouraged not to use the handrail, but were not prohibited from
doing so for safety. A longer time to complete the SCT represents worse functional
limitations. Excellent test-retest reliability (Pearson r=.93) was reported for a similar stair-
climbing task in people with knee OA.37

Radiograph Assessment

Joint alignment.

Tibiofemoral joint alignment was measured from long cassette anterior-posterior (AP)
radiographs that included the hip, knee, and ankle joints. The x-ray tube was centered at the
knee at a distance of approximately 2 m. Participants stood barefoot, with the knees as
straight as possible, and bearing weight on both lower extremities. They were positioned with
the tibial tubercles facing anteriorly. Alignment was measured as the angle formed by the
mechanical axis of the femur and of the tibia38–40 (Fig. 1). The mechanical axes of the femur
and tibia were defined from lines connecting the center of the femoral head to the knee center
and connecting the center of the talus to the knee center, respectively (Fig. 1). An angle of
less than 180 degrees was defined as varus, and an angle of greater than 180 degrees was
defined as valgus. Measurements were done by one author (LCS), and the intraclass
correlation coefficient (ICC) for repeated measurements using these methods was .978.

Figure 1.

Tibiofemoral joint alignment was determined by the angle formed by the intersection of the
mechanical axis of the femur and the mechanical axis of the tibia. The figure shows an angle of less
than 180 degrees, indicating varus alignment.
Frontal-plane knee laxity.

Medial and lateral knee joint laxities were measured using the “open-space” technique41 from
stress radiographs. For the radiographs, participants were positioned supine in a TELOS
stress device* with the knee flexed 20 degrees and the patella facing anteriorly to minimize
limb rotation. The x-ray beam was centered approximately 91 cm above the knee joint. The
TELOS device was used to apply a 150-N force to the joint line to produce opening on the
opposite side of the joint (Fig. 2). Radiographs were adjusted for magnification using a
known distance from the TELOS device that was visible in every image. Joint space was
measured at the narrowest point in the medial and lateral compartments during the
application of varus and valgus forces. Joint laxity was calculated by subtracting the
measured joint space during joint closing from that during joint opening (Fig. 2).
Measurements were made by one author (LCS), and ICC values for repeated measurements
using these methods were .978 for medial laxity and .975 for lateral laxity.

Figure 2.

Setup for varus stress radiograph on left lower extremity, with corresponding radiograph (top). For
the varus stress radiograph (shown), a consistent 150-N force was applied to the medial knee joint
line. For the valgus stress radiograph (not shown), ...

Quadriceps Femoris Muscle Function

Quadriceps femoris muscle force output (in newtons) was measured during a maximal
voluntary isometric contraction (MVIC), with electrical burst superimposition to ensure
maximal quadriceps femoris muscle activation.42 Each participant sat in an isokinetic
dynamometer (Kin Com†) with the knee flexed to 90 degrees, the joint axis aligned with the
dynamometer axis, and the trunk fully supported. Chest, hip, and thigh straps secured the
participant to the chair, and an ankle strap secured the shank to the dynamometer. Following
skin preparation, self-adhesive gel electrodes (7.62×12.70 cm)‡ were secured proximally over
the rectus femoris muscle and distally over the vastus medialis muscle. Each participant
practiced producing maximal quadriceps femoris muscle contractions against the
dynamometer arm while verbal encouragement and visual feedback were provided to
maximize volitional efforts. For the test, participants were asked to produce an MVIC of their
quadriceps femoris muscle, during which a supramaximal burst of electrical current (100
pulses per second, 600-microsecond pulse duration, 10-pulse tetanic train, 130 V) from a
Grass S48 stimulator§ was delivered to the muscle. The burst of electrical current was used
only to assess whether the participants were attempting maximum activation of the
quadriceps femoris muscles.42 The MVIC was the highest volitional force prior to the onset
of the electrical burst. Volitional force production can be influenced by both limb length and
body mass, which may limit group comparisons. In our sample, there was a strong
relationship between height (in meters) and force produced by the quadriceps femoris muscle
during the MVIC (r=.67, P<.001). In order to accurately compare group data, quadriceps
femoris muscle force was normalized by height (in newtons per meter).
Data Analysis

Group differences.

For all variables of interest, means and standard deviations or 95% confidence intervals were
calculated for the self-reported knee instability groups (I0, Im, and If). One-way analyses of
variance were used to evaluate differences among the knee instability groups in age, body
mass index (BMI), radiograph variables, quadriceps femoris muscle force, scores on KOOS
subsets, and time of SCT (dependent variables). Post hoc testing was done with least
significant difference tests, when appropriate. We evaluated the frequency distribution of sex
and radiograph severity (K-L grade II, III, or IV) among the knee instability groups using chi-
square tests of independence.

Relationships among variables.

Relationships among variables were assessed with participants from all groups combined.
The Eta2 statistic was used to evaluate the relationships between self-reported knee instability
(a categorical variable) and medial laxity, limb alignment, and quadriceps femoris muscle
force. Eta2 is a measure of the strength of association between independent and dependent
variables and can be used when one or more variables is categorical in nature. Eta2 is
calculated as: SSbetween/SStotal, where SS is sum of squares. Eta2 describes the amount of
variance in the dependent variable that can be account for by the independent variable, and it
is interpreted like an R2 value.

Separate hierarchical regression analyses were used to predict each of the KOOS subset
scores and scores on the SCT (dependent variables). The independent variables of quadriceps
femoris muscle force, limb alignment, medial laxity, IKOS score, and the interaction between
medial laxity and self-reported knee instability (medial laxity × IKOS score) were entered one
at a time into each regression model. Hierarchical regression is an incremental approach to
multiple regression in which variables are entered into the model based on a priori
hypotheses. It can be performed so that the last variable entered into the model is the
independent variable whose relationship to the dependent variable is unknown. Based on the
literature, relationships have been demonstrated between function and quadriceps femoris
muscle strength,8,11,13 knee alignment,29 and knee laxity.14 In this study, we were interested
specifically in the influence of self-reported knee instability (IKOS score) on the dependent
variables. As such, the IKOS score was entered into the model last in order to assess the
influence of self-reported knee instability after accounting for the influence of the other
independent variables. Thus, quadriceps femoris muscle force was entered into the model
first, followed by limb alignment, then medial laxity, then IKOS score, and finally the
interaction term between medial laxity and IKOS score. The interaction term was calculated by
multiplying the Z-scores for medial laxity and IKOS score. This technique allowed us to
determine the influence of medial laxity, IKOS score or the interaction between the 2 on knee
function after strength and alignment had been accounted for. For all analyses (using SPSS
version 13.0‖), significance was established when the alpha level was ≤.05.

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Results
Group Differences

The frequency of IKOS scores is shown in Table 1. The frequency distribution of sex and K-L
grade within the self-reported knee instability groups was not statistically different (Tab. 2,
P=.630 and P=.744, respectively). On average, the Im group was younger than the other
groups (Tab. 2, P≤.025), but there were no differences among the groups in terms of BMI
(P=.587) (Tab. 2), medial laxity (P=.336), lateral laxity (P=.357), limb alignment (P=.329),
or quadriceps femoris muscle force (P=.453) (Tab. 3). The If group took approximately 4
seconds longer than the I0 group to complete the SCT, but this difference was not statistically
significant (P=.114) (Tab. 3). Significant group differences were observed for all subsets of
the KOOS questionnaire, as those participants reporting worse knee instability also scored
worse on the Pain, Symptoms, ADL, Sport, and QOL subsets (P≤.05, Fig. 3).

Figure 3.

Markers represent average scores on subsets of the Knee Injury and Osteoarthritis Outcome Score
(KOOS) questionnaire (Pain, Symptoms, Quality of Life [QOL], Activities of Daily Living [ADL],
Sport/Recreation [Sport]), ...

Table 3.

Average Data (Standard Deviation) by Self-reported Knee Instability Groupa

Relationships Among Variables

The IKOS score did not relate to medial laxity (Eta2=0.045, P=.336), limb alignment
(Eta2=0.044, P=.329), or quadriceps femoris muscle force (Eta2=0.032, P=.453). Results of
hierarchical regressions are shown in Figure 4. The IKOS score significantly contributed to the
prediction of all KOOS subset scores, even after controlling for quadriceps femoris muscle
force, limb alignment, and medial laxity (Fig. 4). In fact, the IKOS score was the only
significant predictor of Pain, Symptoms, QOL, and ADL subset scores. Both IKOS score and
quadriceps femoris muscle force influenced the prediction of scores on the Sport subset as
well as the SCT. Medial laxity, limb alignment, or the interaction between medial laxity and
IKOS score did not significantly influence the prediction of any functional score.

Figure 4.

Results of hierarchical regression analysis showing the relative contribution (R2 value) of each
variable (vertical bars) in the prediction of scores on subsets of the Knee Injury and Osteoarthritis
Outcome Score (KOOS) questionnaire (Pain, Symptoms, ...

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Discussion
In people with medial knee OA, the aims of our study were: (1) to investigate the relationship
between self-reported knee instability and medial knee laxity, varus alignment, and
quadriceps femoris muscle force; (2) to compare the level of function of participants
classified by reports of knee instability; and (3) to investigate the influences of self-reported
knee instability, medial laxity, varus alignment, and quadriceps femoris muscle force on
function. The results show that self-reported knee instability is not related to medial knee
laxity, mechanical axis, or quadriceps femoris muscle force. The results also demonstrate that
function is worse in individuals who report worse knee instability and that function scores are
predicted by self-reported knee instability, not laxity, even after accounting for the
contribution of quadriceps femoris muscle force. This study is one of the few to investigate
self-reported knee instability in patients with knee OA, and our findings suggest that further
investigation of the causes and impact of self-reported knee instability is warranted.

“Instability” is a term often used clinically to describe the symptom of buckling, shifting, or
giving way of a joint, such as the knee.43 Instability is a sensation experienced by the patient
during dynamic activities, and, in order to evaluate its presence, clinicians rely on patient
reports of buckling, shifting, or giving way. In the biomedical literature, the term “instability”
often is used interchangeably with the term “laxity”; however, their meanings are not the
same. Laxity represents a clinical sign that describes the condition of passive joint
structures43 and is assessed in a static position using an arthrometer or stress device. A
positive finding of increased knee laxity leads many clinicians to presume functional
instability; however, prior to this study, this relationship had not been investigated in people
with knee OA. Our results show no direct relationship between medial laxity and self-
reported knee instability. Furthermore, our results show that the amount of medial knee laxity
is similar between people reporting knee instability and those without knee instability.

Self-reported knee instability, or knee buckling, has been identified only recently as a
significant factor in people with knee OA,26–28 so studies of the mechanisms underlying knee
instability have only just begun. Factors such as increased BMI, ligament laxity, diminished
muscle control, and structural joint changes could contribute to sensations of knee instability,
hence our inclusion of these measures in our work. Our results show no differences among
the self-reported knee instability groups in terms of medial laxity, quadriceps femoris muscle
strength, or tibiofemoral joint alignment. Furthermore, our data showed no direct
relationships between severity of self-reported knee instability and medial laxity, quadriceps
femoris muscle force, or alignment. These findings are in contrast to the findings of Felson et
al,26 who showed that quadriceps femoris muscle weakness and knee pain predicted knee
buckling in people over age 50 years. It is possible that our sample size limited the detection
of differences in quadriceps femoris muscle force, medial laxity, or tibiofemoral alignment
among the instability groups. However, the study by Felson et al included individuals with
and without radiographic evidence of knee OA, so it is possible that different factors may
predict knee buckling in people with OA. It also is likely that self-reported knee instability is
a multifactorial problem, and further investigation of underlying mechanisms is warranted.

In our recent work in patients with medial knee OA, we identified self-reported knee
instability as an important predictor of movement and muscle activation patterns during
walking activities.28,44 In the present study, our results show that self-reported knee instability
is also an important predictor of function. We found that self-reported knee instability
significantly influenced function even after accounting for variables (ie, laxity, alignment,
quadriceps femoris muscle strength) that previously had been associated with decreased
function and disability.8,11,12,29 We utilized the KOOS questionnaire to measure function
because each subset (Pain, Symptoms, ADL, Sport, and QOL) is evaluated as an independent
score. In our sample, individuals with the worse self-reported knee instability (If group)
scored worse on all 5 subsets. Clinically meaningful score changes for the KOOS subsets
have not been established. However, clinically meaningful score changes have been reported
to be 9.7, 9.3, and 10.0 mm for the WOMAC pain, physical function, and stiffness subscales,
respectively.45 Given the close association between the KOOS and the WOMAC, our results
indicate that the difference in scores between the self-reported knee instability groups
(range=10–27 points) represent clinically meaningful differences in function and quality of
life.

Our findings are consistent with those of Fitzgerald et al,27 who reported that a large
percentage of people with medial tibiofemoral, lateral tibiofemoral, and patellofemoral OA
report knee instability that influences function beyond pain, range of motion, and weakness.
Similarly, Felson et al26 reported that people who experienced knee buckling had higher
disability scores on the WOMAC questionnaire independent of pain, weakness, age, and
BMI. Our findings, along with those of Felson et al26 and Fitzgerald et al27 strongly indicate
that self-reported knee instability, or buckling, is an important factor in people with knee OA.
The collective findings signify the importance of assessing and addressing self-reported knee
instability in people with knee OA in order to maximize functional outcomes. Felson et al26
recommended that knee buckling be included in the list of common symptoms in people with
knee problems or OA in medical and rheumatology textbooks.

In this study, participants were classified based on reports of knee instability during activities
of daily living, so it is not surprising that the If group scored worse on the ADL and Sport
subsets of the KOOS questionnaire or that self-reported knee instability was involved in the
prediction of these scores. We defined self-reported knee instability as a sensation of
“shifting, buckling, or giving way” of the knee,31 and none of these items are addressed by
any dimension of the KOOS. Therefore, although both instability and function were
evaluated with self-report measures, we assert that items assessed by the KOOS are separate
and independent from our measure of knee instability and that group differences in function
measured by the KOOS subsets are meaningful. We used the SCT as a performance-based
measure of function. Although small, self-reported knee instability scores significantly
contributed to SCT scores even after accounting for the large influence of quadriceps femoris
muscle force. The If group took approximately 4 seconds longer to complete the task
compared with those participants without self-reported knee instability (I0 group), but this
difference was not statistically significant. There are a number of performance-based
measures of function available to clinicians that were not used in this study, and further
investigation is needed to understand the impact of knee instability on performance-based
measures of function.

Declines in function in people with knee OA have been attributed to both frontal-plane laxity
and knee alignment.14,29 However, we did not find any relationship between medial laxity or
varus alignment with any measure of function. Several methodological differences may
explain the varying results. Work by Sharma and colleagues14 showed that total frontal-plane
laxity was related to decreased function in individuals with medial tibiofemoral, lateral
tibiofemoral, and patellofemoral OA. In the present study, we included only individuals with
medial tibiofemoral OA, so the more homogeneous sample may have influenced the ability to
find a relationship between frontal-plane laxity and knee function. We measured laxity using
stress radiographs during which we applied a 150-N force to the knee joint line with the knee
flexed approximately 20 degrees and the femur and tibia stabilized in a TELOS device.
Sharma et al14 used a custom-designed device that stabilized the thigh, and they produced
varus-valgus motion by applying a 40-N force to the foot, which may have resulted in
different frontal-plane laxity measurements. In the present study and in the study by Lewek et
al,46 stress radiographs were used to allow the medial and lateral sides of the joint to be
assessed separately. It often is presumed that excessive frontal-plane motion is the result of
ligament strain on the lateral side of the joint and cartilage erosion on the medial side. Lewek
et al46 demonstrated, however, that lateral laxity is no different in people with medial knee
OA, whereas medial laxity is greater than that in age and sex-matched control subjects. It is
important to identify the source of increased frontal-plane motion in this patient population.

In our sample, those participants who reported knee instability (Im and If groups) reported
worse knee symptoms, such as clicking/grinding and swelling, than those who never
experience knee instability. This finding may suggest that patients with worse instability also
have more-severe OA, based on clinical presentation. Clinical severity of knee OA does not
always correlate with radiographic severity of the disease, and we did not find any
differences among the groups in terms of frequency of radiographic severity of OA.
However, joint instability can be associated with higher shear forces in the knee that are
particularly damaging to articular cartilage.47,48 Longitudinal investigations with larger
sample sizes are necessary to further understand the relationship between self-reported knee
instability and joint integrity.

Our sample was inclusive of individuals with only medial knee OA of an idiopathic origin.
We do not know whether the disease course of idiopathic (or primary) OA differs from that
of secondary OA, so we excluded those individuals who reported a history of a possible
ligament injury in order to ensure a more homogeneous sample. Idiopathic knee OA is more
prevalent in women49; however, this was not reflected in the distribution of men and women
in our sample. Our inclusion of individuals with only medial knee OA may have altered the
expected distribution of male and female participants. Although the exact nature of self-
reported knee instability in this patient population is unknown, we chose to exclude potential
participants with patellofemoral joint disease in order to limit the possibility of instability
arising from the patellofemoral joint. Despite the homogeneity of our sample, these findings
may provide insight into the influence of self-reported knee instability for individuals with
knee OA in other or multiple compartments.

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Conclusion
This study showed that in people with medial knee OA, self-reported knee instability is a
problem that does not have a direct association with medial laxity, quadriceps femoris muscle
weakness, and varus alignment. In addition, self-reported knee instability can influence
function over and above that explained by laxity, weakness, and malalignment. We
acknowledge that there are several other factors that may contribute to function that were not
included in this study. Although our work is preliminary, the findings indicate that self-
reported knee instability, or the factors that contribute to knee instability, may need to be
addressed in rehabilitation of people with medial knee OA in order to maximize function. We
have shown that self-reported knee instability significantly influences movement and muscle
activation patterns during walking activities.28,44 Further investigation of self-reported knee
instability and neuromuscular control of the knee may expound the multifactorial nature of
self-reported knee instability. Further investigation also is necessary to reproduce these
findings with larger sample sizes and to evaluate the long-term consequences of self-reported
knee instability on joint integrity.

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Supplementary Material
[The Bottom Line]

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Notes
Dr Schmitt, Dr Fitzgerald, and Dr Rudolph provided concept/idea/research design. Dr
Schmitt and Dr Rudolph provided writing and data analysis. Dr Schmitt provided data
collection. Dr Rudolph provided project management, fund procurement, and
facilities/equipment. Dr Reisman provided participants. Dr Fitzgerald and Dr Reisman
provided consultation (including review of manuscript before submission). The authors
acknowledge Papastavros Medical Imaging for assistance with radiographs and Michael Axe,
MD, for assistance with participant recruitment.

This research, in part, was presented at the Combined Sections Meeting of the American
Physical Therapy Association; February 1–5, 2006; San Diego, California.

This research was funded by grant P20-RR016458 from the National Center for Research
Resources (NCRR), a component of the National Institutes of Health (NIH), by NIH grant
T32-HD007490, and by Foundation for Physical Therapy Promotion of Doctoral Studies II
(PODS II) Awards (2004-2005, 2005-2006).
*
Austin & Associates, 1109 Sturbridge Rd, Fallston, MD 21047.
†
Isokinetic International, 6426 Morning Glory Dr, Harrison, TN 37341.
‡
ConMed Corp, 525 French Rd, Utica, NY 13502.
§
Grass Instrument Division, Astro-Med Inc, 600 East Greenwich Ave, West Warwick, RI
02893.
‖
SPSS Inc, 233 S Wacker Dr, Chicago, IL 60606.

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