Symposium-Rheumatology

An approach to monoarthritis
Molly Mary Thabah, Maj. Gen. Ved Chaturvedi1

Abstract
Monoarthritis can be inflammatory or non-inflammatory, and can be acute or chronic. A thorough history and
physical examination can differentiate inflammatory from non-inflammatory monoarthritis. The most common
causes of acute inflammatory monoarthritis are infectious arthritis, crystal induced arthritis (gout and pseudogout).
Examination of synovial fluid often is essential in making a definitive diagnosis. Immunoinflammatory diseases
like rheumatoid arthritis, systemic lupus erythematosus, spondyloarthritis, Behçet’s disease, and reactive arthritis
can all begin as acute inflammatory monarthritis. Synovial biopsy is useful to diagnose chronic infections like
tuberculosis and brucellosis. In order to arrive at a final diagnosis other organ systems should be thoroughly
reviewed, because other systemic illness like sickle cell disease, thalassemia, sarcoidosis can all cause
monoarthritis.

Keywords: Monoarthritis, monoarticular pain, crystal induced arthritis, gout, pseudogout

Introduction 1. Therefore the first step in approach to a patient

Musculoskeletal diseases are among the most
common reasons for which medical help is sought.
Anywhere between 25% and 30% individuals will
have a musculoskeletal complaints in their life time.
[1,2]
A significant proportion of patients who present
with musculoskeletal complaints have in fact systemic
illness such as rheumatoid arthritis (RA), systemic lupus
erythematosus (SLE) etc. which may be potentially
life-threatening if not detected, correctly diagnosed
and treated. These conditions have to be distinguished
from other musculoskeletal conditions, which have no
systemic component, are mechanical in origin and are
referred to the orthopedic department.[3]
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with musculoskeletal complaints is to separate
systemic, serious, life-threatening illness from
local, regional and mechanical problems.[3] Patients
with musculoskeletal problems could have any of
the following presenting complaints.
• Joint pain/arthralgia.
• Arthritis.
• Diffuse pain.
• Stiffness of joints.
• Back pain.
• Constitutional symptoms.
• Symptoms of systemic organ, muscular or
cutaneous involvement.
2. The next step in approach to a patient with
musculoskeletal complaints is to find out from which
structure this pain is arising from (anatomical basis).
Pain could arise from the joint or from periarticular
structures (articular versus non-articular). Articular
structures include the synovium, synovial fluid,
articular cartilage, intra-articular ligaments, joint
capsule and juxta-articular bone. Non-articular (or
peri-articular) structures, such as supportive extra-

Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, 1 Consultant
Rheumatologist, AMC Centre and College, Lucknow, Uttar Pradesh, India

Address for correspondence:

Dr. Molly Mary Thabah, Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research,
Puducherry - 605 006, India. E-mail: mthabah@yahoo.com

Journal of Mahatma Gandhi Institute of Medical Sciences March 2014 | Vol 19 | Issue 1
Thabah and Chaturvedi: Monoarthritis 13

articular ligaments, tendons, bursa, muscle, fascia, Therefore, monoarthritis which is arthritis of a single
bone, nerve and overlying skin, may be involved in joint can either be acute or chronic or be either
the pathologic process. inflammatory or non-inflammatory.
Articular disorders may be characterized by deep or
diffuse pain, pain on active and passive movement and Acute Inflammatory Monoarthritis
swelling (caused by synovial proliferation, effusion,
or bony enlargement), crepitation, instability, or Acute inflammatory monoarthritis is a rheumatology
deformity. By contrast, non-articular disorders tend emergency. The most important causes are infectious
to be painful on active, but not passive movement, (septic) arthritis, acute gouty arthritis, pseudogout,
demonstrate focal tenderness and swelling away from reactive arthritis and initial presentation of a
the joint line. Moreover, non-articular disorders may polyarthritis.[4] The diagnosis of septic arthritis should
rarely have synovitis, swelling, crepitus, instability, or not be missed as delay in initiating antibiotic therapy
deformity of the joint itself. can lead to permanent damage to the cartilage of
Pain caused by bone diseases can be difficult to the joint. History must include history of fever and
distinguish from that from the joints. Examples of involvement of other joints. Presence of classical
diffuse bone diseases are metabolic bone disease, signs of inflammation-red hot swollen and tender joint
multiple myeloma and multi focal osteomyelitis. makes it easy to label acute inflammatory arthritis.
In general bone diseases cause pain which is much Synovial fluid analysis is the single most important test
worse at night. This category must also be considered in the emergency evaluation of acute monoarticular
in differential diagnosis of musculoskeletal pain. arthritis.[5] Synovial fluid should be sent for cell count,
3. Once articular origin of the pain is established, the gram stain, bacterial culture and also examined for
other relevant features include the duration (acute crystals under polarized light microscope.
<6 and chronic >6 weeks); the number (mono, a. Non gonococcal bacterial arthritis (septic
oligo (≤3), or polyarthritis), and distribution arthritis) — Septic arthritis is a true rheumatology
of joint involvement, and whether the pain is emergency because it can rapidly destroy the
inflammatory (morning stiffness >30 min, systemic articular cartilage.[6] Septic arthritis may develop
symptoms, local inflammatory signs, laboratory in a fulminant fashion with high grade fever,
evidence of inflammation- (elevated ESR/ CRP, confusion and marked toxicity or may be subacute
thromobocytosis, anaemia of chronic disease, etc.) with little or no fever. The knee joint is the most
or non-inflammatory. common joint to be involved, followed by hip and
Therefore a patient with arthritis (joint pain and less commonly are the shoulder, wrist and elbow.
swelling) can be classified in one of the categories Patients with RA are at increased of developing
as given in Table 1.[3] septic arthritis.[7] Prior joint abnormality, prosthetic
joint also significantly increases the likelihood
Table 1: Shows a broad classification of the causes of developing septic arthritis.[8] It is important
of arthritis with a focus on major causes to rule out septic arthritis in any patient of RA
of monoarthritis who presents with a red hot and swollen joint.[8]
Acute arthritis Chronic arthritis Synovial fluid typically reveal white cell count of
Inflammatory
>50,000 cells/µL. Staphylococcus aureus is still
Monoarthritis Monoarthritis
Crystal induced arthritis Tubercular arthritis the most common cause of non-gonococcal septic
(gout and pseudogout) Fungal arthritis arthritis. Other pathogens include Streptococcus
Septic arthritis Other infections (e.g Brucellosis)
Gonococcal arthritis Immunoinflammatory arthritis
pneumoniae and Gram-negative bacilli. Reports
Acute onset of inflammatory Crystal induced arthritis in the literature show an increased incidence of
polyarthritis (like RA, SLE) methicillin-resistant S. aureus.[9]
Polyarthritis (e.g., acute onset Polyarthritis (e.g., RA, psoriatic
of polyarthritis, reactive arthritis) arthritis, spondyloarthritis)
Treatment for septic arthritis consists of hospital
Non-inflammatory admission and appropriate empirical intravenous
Monoarthritis Monoarthritis (IV) antibiotics (also to cover for S. aureus) should
Hemarthrosis Single joint osteoarthritis be started once samples for gram stain and culture
Trauma Neuropathic arthropathy
Osteonecrosis has been obtained to avoid joint destruction. Daily
Pigmented villo nodular synovitis aspiration should be done for accessible joints like
Polyarthritis Polyarthritis (e.g., osteoarthritis) the knee. Orthopedic consultation should be sought

March 2014 | Vol 19 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
14
because certain joints such as shoulder and hip may
require arthrotomy and open drainage. There is no
role of intra-articular antibiotics.
b. Gonococcal arthritis is main cause of infectious
arthritis in young persons (<40 years of age).[10]
The causative organism is Neisseria gonorrhoeae
and arthritis is a consequence of bacteremia arising
from gonococcal infection or, more frequently, from
asymptomatic gonococcal mucosal colonization
of the urethra, cervix, or pharynx. Women are at
greatest risk during menses and during pregnancy
and overall are two to three times more likely than
men to develop disseminated gonococcal infection
(DGI) and arthritis.
DGI is a syndrome of fever, chills, rash and arthritis
which is migratory, with prominent tenosynovitis of
the knees, hands, wrists, feet and ankles. Important
findings on the skin of the trunk and extensor
surface of extremities are papules that progress to
hemorrhagic pustules.
True gonococcal septic arthritis is a monoarthrits of
hip, knee, ankle, or wrist. Gonococcal septic arthritis
is less common than the DGI syndrome and always
follows DGI, which is unrecognized in one-third of
patients. Synovial fluid, typically contains >50,000
leukocytes/L; the gonococcus is only occasionally
evident in gram-stained smears and cultures of
synovial fluid are positive in <40% of cases. Blood
cultures are almost always negative. Treatment
consists of ceftriaxone (1 g IV or intramuscular
every 24 h) to cover possible penicillin-resistant
organisms, until resolution of local and systemic
signs. This can be followed by oral ciprofloxacin
(500 mg twice daily) to complete 10-14 day course.
c. Crystal induced arthritis — Gout, which is caused
by monosodium urate crystals, is the most common
type of inflammatory monarthritis.[11, 12] Gout occurs
almost always in a man above the age of 40 years.
In general, only one joint is affected initially, but
polyarticular acute gout can occur in subsequent
episodes. The metatarsophalangeal joint of the
first toe often is involved, but tarsal joints, ankles
and knees also are affected commonly. The first
episode of acute gouty arthritis frequently begins
at night with dramatic joint pain and swelling.
The pain may be so excruciating that the patient
may not even tolerate the touch of the bed clothes.
Joints rapidly become warm, red and tender and
there may be peeling of skin overlying the affected
joint with a clinical appearance that often mimics
that of cellulitis. Early attacks tend to subside
Journal of Mahatma Gandhi Institute of Medical Sciences March 2014 | Vol 19 | Issue 1
Thabah and Chaturvedi: Monoarthritis
spontaneously within 3 to 10 days and most of the
patients have intervals of varying length with no
residual symptoms until the next episode. Later
attacks may be monarticular or polyarticular.
Certain events may precipitate acute gouty
arthritis-these include excessive alcohol intake,
dietary excess, trauma and surgery.
d. Pseudogout — Calcium pyrophosphate dihydrate
crystals can cause monoarthritis that is clinically
indistinguishable from gout and thus is often called
pseudogout. Pseudogout is most common in the knee
and wrist, but it has been reported in a variety of
other joints, including the first metatarsal phalangeal
joint (MTP) joint. Among other crystals known to
cause acute mono-arthritis are apatites, calcium
oxalate and liquid lipid crystals.
Chronic Inflammatory Monoarthritis
The causes of chronic inflammatory monoarthritis
are indolent infections such as tuberculosis (TB),
brucellosis, fungal infections and rare parasitic
infections. Any patient who presents with the chronic
inflammatory monoarthritis must undergo synovial
fluid analysis especially for microbiological analysis
and/or synovial biopsy must be done in order to get
a correct diagnosis. Other important causes of chronic
inflammatory monoarthritis are tophaceous gout and
immunoinflamatory arthritis due to autoimmune
conditions like spondyloarthritis (SpA), SLE or RA.
By and large this category remains a diagnosis of
exclusion.
a. Tubercular arthritis — Approximately 10-11%
of extrapulmonary TB involves bone and joints
(osteoarticular TB).[13] The most common site of
osteoarticular TB is the spine, followed by peripheral
tubercular arthritis.[14] Tubercular arthritis occurs
mainly as a chronic monoarticular arthritis of a hip
or knee (about 85%), but may involve other joints.
[14]
The onset of tubercular arthritis is typically
insidious with pain and swelling of a single
joint, but signs of inflammation may be limited.
Tubercular arthritis is usually due to reactivation
of a hematogenously seeded focus and need not
be associated with active disease elsewhere; it
can also spread from adjacent osteomyelitis. The
risk factors for development of osteoarticular TB
and include individuals who are from low socio-
economic status, alcoholics, diabetes mellitus, HIV
infection, corticosteroid therapy and other chronic
illnesses.
Thabah and Chaturvedi: Monoarthritis
TB of the hip usually presents with mild to
moderate pain in the groin, thigh or knee. Children
most commonly presents with a limp. At rest the
hip is usually held in a flexed and abducted posture.
It is common to find atrophy of gluteal muscles and
tenderness in the groin. Plain radiographs in early
stage of the disease are non-diagnostic, but in later
stages of the disease there can be destruction of the
femoral neck, acetabulum and cold abscess.
TB of the knee usually presents with insidious onset
pain, swelling and stiffness. Other presentations
include a limp and reduction in motion of the knee.
The joint is usually warm to touch; synovitis and
effusion are commonly present. Muscle spasm and
synovial effusion result in flexion deformity. Plain
radiographs in the early stage of disease will show
soft-tissue swelling subsequently damage to the
articular cartilage will result in narrowing of the
joint space, irregularity of the cartilage surface and
areas of destruction of the epiphysis.
A high index of suspicion is necessary for early
diagnosis. Yield of synovial fluid smear for acid
fast bacilli is only 20-40%, while culture may
become positive in up to 80% of cases.[13] Synovial
fluid analysis shows elevated cell counts with no
specific distinguishing features. Very low glucose
levels in synovial fluid may favor the diagnosis of
TB. Synovial biopsy is a must in cases of chronic
monoarticular inflammatory arthritis where
diagnosis is in doubt.
Treatment of tubercular arthritis is same as for
other forms of TB. The intensive phase consists
of administration of rifampicin, isoniazid,
pyrazinamide and ethambutol for 2 months,
followed by a continuation phase of rifampicin
and isoniazid for 4 months. Intermittent short
course chemotherapy has not been assessed in
osteoarticular TB. The optimal duration of therapy
is also still unsettled.[13] Hence, each patient has
to be individually assessed and where relevant,
treatment duration may have to be extended for a
given patient.[15]
b. Fungal infections — Fungal arthritis is a rare but
nevertheless an important differential diagnosis of
chronic monoarthritis. It usually follows a chronic
indolent course of several months that leads to
delays in diagnosis and to inappropriate treatment
such as intra-articular and systemic steroids.
[16]
Various predisposing factors that depress the
immune system have been implicated in patients
developing fungal arthritis.
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15
Candida species can rarely cause septic arthritis.[17]
Isolated monoarthritis is caused by the direct intra-
articular inoculation of fungi that inhabit the skin or
as a complication of hematogenously disseminated
candidiasis. Disseminated candidiasis with its
accompanying arthritis is seen in patients with
serious underlying disorders, IV drug abusers or
after prolonged antibiotic therapy.[18] Rare cases have
been reported where direct inoculation is caused by
repeated injection of a joint or as a contaminant
during joint surgery.[19,20] The causative organism
in 80% of cases is Candida albicans and remaining
cases are caused by Candida tropicalis.[21] The knee
is the most commonly affected joint in most cases,
though any other peripheral joint or the spine can
also be affected.[21] Most cases are monoarticular and
osteomyelitis is often present. Diagnosis is achieved
by isolating the organism by culture of the aspirated
joint fluid or bone. Treatment with amphotericin B is
effective and joint destruction with loss of function
occurs only in a small percentage of affected
individuals.
Coccidioides immitis, Blastomyces dermatitidis
and Histoplasma capsulatum are rare causes of
chronic monoarthritis.[16] Arthritis due to these
dimorphic fungus results from hematogenous
seeding or direct extension from bony lesions in
persons with disseminated disease.
Infection with Sporothrix schenckii is common
among gardeners and other persons who work
with soil or sphagnum moss. Joint involvement is
rare.[22] Articular sporotrichosis is six times more
common among men than among women and
alcoholics and other debilitated hosts are at risk for
polyarticular infection.[23] Tenosynovitis, with or
without carpal tunnel syndrome, is associated with
deep inoculations. If untreated, the infection will
lead to osteomyelitis.
c. Immunoinflammatory causes of chronic
inflammatory monoarthritis. The SpA group
of diseases consists of ankylosing spondylitis
(AS), reactive arthritis, psoriatic arthritis (PsA),
arthropathies associated with inflammatory bowel
disease (IBD) and undifferentiated SpA.[24] A
pattern of peripheral arthritis which is asymmetrical,
oligoarticular and predominantly of lower limb is
characteristic of this group of diseases.[24]
Diagnosis of SpA in a patient with chronic
monoarthritis is suggested by presence
inflammatory back pain or enthesitis or
dactylitis, with one SpA feature like; psoriasis,
16
IBD, preceding infection, HLA-B27, uveitis,
inflammatory sacroiliitis on magnetic resonance
imaging or plain radiographs.[25, 26]
Peripheral arthritis in AS predominantly involves
the lower extremities, especially the knee.[27,28]
Reactive arthritis commonly presents with
monoarthritis of ankle or knee. History of preceding
infection either urethritis can be elicited in 40%
cases. Synovial fluid will not show any organism.[29]
Other immunoinflammatory systemic diseases that
may be associated with chronic monarticular arthritis
are RA, SLE, Behçet’s disease.
Therefore since indolent infections like TB, brucellosis
and fungal infections constitute a major portion of
chronic inflammatory monoarthritis synovial fluid
microbiology and/or biopsy must be performed to get
the actual diagnosis.
Acute Non-inflammatory Monoarthritis
The causes of acute non-inflammatory monoarthritis
would include trauma, bleeding in to the joint
(hemarthrosis) and palindromic rheumatism.
Trauma to a joint can lead to internal derangement,
hemarthrosis, or fracture. Such patients should be
evaluated with plain radiographs and referred to the
orthopedic surgeon. Penetrating injuries from thorns,
wood fragments, or other foreign materials can cause
non-inflammatory monoarthritis.[30,31] There are case
reports of foreign body in the joint (foreign body
synovitis) presenting like septic arthritis.
Hemarthrosis
The most common causes of hemarthrosis is congenital
disorders such as hemophilia.[32] Hemophilia is a sex-
linked recessive genetic disorder characterized by the
absence or deficiency of factor VIII (hemophilia A,
or classic hemophilia) or factor IX (hemophilia B, or
Christmas disease). Spontaneous acute hemarthrosis
occurs commonly with both types of hemophilia.
Recurrent spontaneous accumulation of blood in to the
joint can lead to a deforming arthritis.[32] Hemarthrosis
is not common in other disorders of coagulation such as
von Willebrand disease, factor V deficiency, warfarin
therapy, or thrombocytopenia.
Hemarthrosis occurs when the child begins to walk and
run. The joints most commonly affected are the knees,
ankles, elbows, shoulders and hips. In the acute stage
of bleeding the joint is warm, swollen and tender. The
patient holds the affected joint in flexion and guards
Journal of Mahatma Gandhi Institute of Medical Sciences March 2014 | Vol 19 | Issue 1
Thabah and Chaturvedi: Monoarthritis
against any movement. Blood in the joint is resorbed
over a period of a week or longer and pain, swelling
and tenderness decreases. Recurrent hemarthrosis
result in chronic arthritis, where swelling persists and
deformity of the joint develops.
The diagnosis of hemarthrosis should be considered
in a young male who presents with recurrent swollen
and painful joint, which gradually improves on its
own overtime. The treatment of hemarthrosis consists
of immediate infusion of factor VIII or IX at the first
sign of joint or muscle hemorrhage. Pain relief with
paracetamol or Cox-2 inhibitors should be given,
non-selective nonsteroidal anti-inflammatory drugs
are generally avoided because of theoretical risk of
potentiating the bleeding.
Chronic Non-inflammatory
Monoarthritis
Under this heading is single joint osteoarthritis (OA),
osteonecrosis, neuropathic joint and pigmented
villonodular synovitis (PVNS).
a. OA is the most common type of arthritis. World-
wide estimates indicate that 9.6% of men and 18%
of women >60 years have symptomatic OA.[1] It
is a heterogeneous group of disorders with shared
clinical features that bind the group together. OA
can be primary or secondary based on the presence
or absence of an obvious cause. It can be localized
or generalized based on the distribution between
joints and numbers of joints involved. Knee OA
is very common and is often associated with
disability.[33] Symptomatic hip OA is one-third as
common as disease in the knee.
The two cardinal symptoms of OA are joint pain
that worsens with use and difficulty initiating joint
movement after inactivity (also known as gelling
of the joints).
The joint affected by OA generally has evidence of
mild to — moderate firm swelling around the joint
line due to osteophytes at the joint margin, palpable
crepitus and restricted range of motion with pain
at the end of the range. Other common findings on
clinical examination are weakness and wasting of
the muscles acting on the joint, tenderness around
the joint and deformities and instability of the joints
are seen in late stages.
b. Neuropathic arthropathy — Joint disease secondary
to neuropathy was first described by Jean Marie
Charcot, hence it also known as Charcot arthropathy.
Thabah and Chaturvedi: Monoarthritis
It was most commonly described in association
with tertiary syphilis, however nowadays it most
commonly occurs due to diabetic neuropathy.[34]
Other causes of neuropathic arthropathy are spinal
cord diseases such as syringomyelia, spinabifida,
spinal cord injuries.[35] The loss of pain sensation,
proprioception and abnormal muscular reflexes
that modulate joint movement leads to repeated
trauma, resulting in progressive cartilage and bone
damage.
Neuropathic arthropathy may present as an acute
or subacute monoarthritis with swelling, erythema
and variable amounts of pain in the affected joint.
Chronic presentation often mimics OA. The
most important clinical findings in neuropathic
arthropathy are the presence of a significant
sensory deficit and a degree of pain that is less than
would be expected considering the amount of joint
destruction evident on radiographs.
The pattern of joint involvement depends on the
location of the neurologic impairment and may
involve small as well as large joints. In diabetes,
the foot is most commonly involved. Patients
with syringomyelia typically demonstrate upper
extremity involvement.[36]
c. Osteonecrosis also known as avascular necrosis is
characterized pathologically by presence of dead
bone can present like arthritis. The most common
site for involvement is the femoral head. Other
sites are knee, ankles, shoulders and elbows.
The most common risk factor for osteonecrosis
is glucocorticoid use.[37] An important scenario
is development of pain of the groin, typically a
deep, throbbing pain in a patient with rheumatic
illness who is on glucocorticoids. This pain which
is worse at night is usually intermittent and of
gradual onset, occasionally appears abruptly.
Osteonecrosis is often seen in RA, SLE, systemic
vasculitis and other rheumatic illness, the major risk
factor being glucocorticoid therapy. Other causes
include fracture, dislocation, radiation injury,
pregnancy, sickle cell disease, coagulopathies,
hemoglobinopathies, organ transplantation,
myeloproliferative diseases etc.
d. Pigmented villo nodular synovitis (PVNS) is a
rare non-inflammatory proliferative disorder of the
synovium with deposition of pigment in the tissue.
The etiology is unknown. The term PVNS was
introduced in 1941 by Jaffe, Lichtenstein and Sutro
to describe a ‘yellow-brown tumor-like tenosynovial
lesion’.[38] The typical patient is 20-40 years old male
March 2014 | Vol 19 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
17
who complaints of a traumatic swelling of a single
joint.[38] The knee is involved 80% of the time. The
synovial fluid is almost always gross red or bloody.
Diagnosis is established by biopsy of the synovium,
which is defined by the presence of giant cells, foamy
cells and hemosiderin deposits in synovial tissue.
Conclusions and Pearls for Diagnosis
• Pain and swelling (arthritis) of a single joint requires
prompt evaluation to identify septic arthritis, crystal
induce arthritis and acute onset of inflammatory
polyarthritis.
• Acute inflammatory monoarthritis is infection
unless proved otherwise.
• Synovial fluid analysis is the most important
investigation in the evaluation of both acute and
chronic monoarthritis.
• Septic arthritis can rapidly destroy the joint if not
detected and promptly treated.
• Septic arthritis can be superimposed on gout and
pseudogout.
• Gonococcal arthritis is seen in a young person.
• Serum uric is often normal during an acute attack of
gout; diagnosis of gout requires the demonstration
of intracellular monosodium urate crystals in the
joint fluid under polarized light microscope.
• RA, SLE, IBD associated arthritis, PsA, Behçet’s
disease and reactive arthritis can all begin as acute
inflammatory monarthritis.
• Other systemic diseases associated with acute
inflammatory monoarthritis are sarcoidosis, sickle
disease, hemoarthrosis due to hemophilia and
arthritis associated with chronic viral infections.
• Tuberculosis and other indolent infections should
be considered in the differential diagnosis of
chronic inflammatory monoarthritis. Synovial
biopsy must be performed to get the diagnosis.
• Osteonecrosis, OA, neuropathic joint and PVNS
should be considered in the differential diagnosis
of chronic non-inflammatory monoarthritis.
References
1. Woolf AD, Pfleger B. Burden of major musculoskeletal
conditions. Bull World Health Organ 2003;81:646-56.
2. Woolf AD, Akesson K. Understanding the burden of
musculoskeletal conditions. The burden is huge and not
reflected in national health priorities. BMJ 2001;322:1079-80.
3. Malaviya AN. A patient with musculoskeletal (MSK) pains-
clinical approach. Bull Kuwait Inst Med Spec 2004;3:73-82.
4. Suresh E. Problem based review: The patient with acute
monoarthritis. Acute Med 2013;12:111-6.
18
5. Li SF, Henderson J, Dickman E, Darzynkiewicz R. Laboratory
tests in adults with monoarticular arthritis: Can they rule out
a septic joint? Acad Emerg Med 2004;11:276-80.
6. Goldenberg DL. Septic arthritis. Lancet 1998;351:197-202.
7. Favero M, Schiavon F, Riato L, Carraro V, Punzi L. Rheumatoid
arthritis is the major risk factor for septic arthritis in
rheumatological settings. Autoimmun Rev 2008;8:59-61.
8. Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD,
van de Laar MA. Risk factors for septic arthritis in patients
with joint disease. A prospective study. Arthritis Rheum
1995;38:1819-25.
9. Frazee BW, Fee C, Lambert L. How common is MRSA in adult
septic arthritis? Ann Emerg Med 2009;54:695-700.
10. García-De La Torre I, Nava-Zavala A. Gonococcal and
nongonococcal arthritis. Rheum Dis Clin North Am
2009;35:63-73.
11. Richette P, Bardin T. Gout. Lancet 2010;375:318-28.
12. Schumacher HR. Crystal-induced arthritis: An overview. Am J
Med 1996;100:46S-52.
13. Malaviya AN, Kotwal PP. Arthritis associated with tuberculosis.
Best Pract Res Clin Rheumatol 2003;17:319-43.
14. Sequeira W, Co H, Block JA. Osteoarticular tuberculosis:
Current diagnosis and treatment. Am J Ther 2000;7:393-8.
15. Sharma SK, Mohan A. Extrapulmonary tuberculosis. Indian J
Med Res 2004;120:316-53.
16. Cuéllar ML, Silveira LH, Espinoza LR. Fungal arthritis. Ann
Rheum Dis 1992;51:690-7.
17. Katzenstein D. Isolated Candida arthritis: Report of a case and
definition of a distinct clinical syndrome. Arthritis Rheum
1985;28:1421-4.
18. Graham DR, Frost HM. Candida guilliermondi infection of
the knee complicating rheumatoid arthritis: A case report.
Arthritis Rheum 1973;16:272-7.
19. Levine M, Rehm SJ, Wilde AH. Infection with Candida albicans
of a total knee arthroplasty. Case report and review of the
literature. Clin Orthop Relat Res 1988; 226:235-9.
20. Dutronc H, Dauchy FA, Cazanave C, Rougie C, Lafarie-Castet
S, Couprie B, et al. Candida prosthetic infections: Case series
and literature review. Scand J Infect Dis 2010;42:890-5.
21. Fainstein V, Gilmore C, Hopfer RL, Maksymiuk A, Bodey GP.
Septic arthritis due to Candida species on patients with
cancer: Report of five cases and review of the literature. Rev
Infect Dis 1982;4:78-85.
22. Appenzeller S, Amaral TN, Amstalden EM, Bertolo MB,
Neto JF, Samara AM, et al. Sporothrix schenckii infection
presented as monoarthritis: Report of two cases and review
of the literature. Clin Rheumatol 2006;25:926-8.
23. Kauffman CA, Bustamante B, Chapman SW, Pappas PG,
Infectious Diseases Society of America. Clinical practice
guidelines for the management of sporotrichosis: 2007
update by the Infectious Diseases Society of America. Clin
Infect Dis 2007;45:1255-65.
Journal of Mahatma Gandhi Institute of Medical Sciences March 2014 | Vol 19 | Issue 1
Thabah and Chaturvedi: Monoarthritis
24. Zochling J, Brandt J, Braun J. The current concept of
spondyloarthritis with special emphasis on undifferentiated
spondyloarthritis. Rheumatology (Oxford) 2005;44:1483-91.
25. Rudwaleit M, van der Heijde D, Landewé R, Listing J,
Akkoc N, Brandt J, et al. The development of Assessment of
SpondyloArthritis international Society classification criteria
for axial spondyloarthritis (part II): Validation and final
selection. Ann Rheum Dis 2009;68:777-83.
26. Rudwaleit M, van der Heijde D, Landewé R, Akkoc N, Brandt
J, Chou CT, et al. The Assessment of SpondyloArthritis
International Society classification criteria for peripheral
spondyloarthritis and for spondyloarthritis in general. Ann
Rheum Dis 2011;70:25-31.
27. Sieper J, Braun J, Rudwaleit M, Boonen A, Zink A. Ankylosing
spondylitis: An overview. Ann Rheum Dis 2002;61:iii8-18.
28. Aggarwal R, Malaviya AN. Clinical characteristics of patients
with ankylosing spondylitis in India. Clin Rheumatol 2009;28:
1199-205.
29. Carter JD, Hudson AP. Reactive arthritis: Clinical aspects and
medical management. Rheum Dis Clin North Am 2009;35:21-44.
30. O’Connor CR, Reginato AJ, DeLong WG Jr. Foreign body
reactions simulating acute septic arthritis. J Rheumatol
1988;15:1568-71.
31. Kandel L, Friedman A, Chaimski G, Howard C, Mann G, Lowe
J. Foreign-body synovitis mimicking septic arthritis of the
knee. Arthroscopy 2001;17:993-6.
32. Upchurch KS, Brettler DB. Hemophilic arthropathy. In:
Firestein GS, Budd RC, Gabriel SE, McInnes IB, O’Dell
JR, editors. Kelley’s Textbook of Rheumatology. 9th ed.
Philadelphia: Elsevier Saunders; 2012. p. 1915-23.
33. Peat G, McCarney R, Croft P. Knee pain and osteoarthritis in
older adults: A review of community burden and current use
of primary health care. Ann Rheum Dis 2001;60:91-7.
34. Rogers LC, Frykberg RG, Armstrong DG, Boulton AJ, Edmonds
M, Van GH, et al. The Charcot foot in diabetes. Diabetes Care
2011;34:2123-9.
35. Turkiewicz AM, Kerr G. Clinical images: Syrinx-induced
Charcot shoulder. Arthritis Rheum 2004;50:2380.
36. Aly AR, Rajasekaran S, Obaid H, Bernacki B. Bilateral
ulnar neuropathy at the elbow secondary to neuropathic
arthropathy associated with syringomyelia. PM R
2013;5:533-8.
37. Weinstein RS. Glucocorticoid-induced osteonecrosis.
Endocrine 2012;41:183-90.
38. Bentley G, McAuliffe T. Pigmented villonodular synovitis. Ann
Rheum Dis 1990;49:210-1.
How to cite this article: Thabah MM, Chaturvedi V. An approach
to monoarthritis. J Mahatma Gandhi Inst Med Sci 2014;19:12-8.
Source of Support: Nil, Conflict of Interest: None declared.