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1. Inflammatory Arthritis
MODERATED BY: PREPARED BY:
DR. P. TAHBILDAR DR.S.H.RANNA
PROF&HOD,ORTHO PGT,ORTHO
15-06-2016

2. Objectives
• Review the history and physical
examination findings of inflammatory
arthritis.
• Define and categorize inflammatory
arthritis.
• Initial laboratory and radiological
evaluation of suspected disease.
• Management of the disease.

3. The Rheumatologic History
• presenting complaints - Onset
- progression
- distribution of disease
- stiffness
- aggravating or relieving factor
- diurnal variation
- other systemic feature
- functional disability
• General systematic medical history.
• Past medical and surgical history.
• Family history.
• Drug history.

4. Inflammatory Vs.Mechanical
Feature Inflammatory Mechanical
Morning stiffness >1 h < 30 min
Fatigue Profound Minimal
Activity Improves Worsens
Rest Worsens Improves
Systemic Yes No
Corticosteroid Yes No

5. Inflammatory Vs. Noninflammatory
Feature Inflammatory Noninflammatory
Pain (when?)
Swelling
Erythema
Warmth
AM stiffness
Systemic features
î ESR, CRP
Synovial fluid
WBC
Examples
Yes (AM)
Soft tissue
Sometimes
Sometimes
Prominent
Sometimes
Frequent
WBC >2000
Septic, RA, SLE,
Gout
Yes (PM)
Bony
Absent
Absent
Minor (< 30 ‘)
Absent
Uncommon
WBC < 2000
OA, AVN

6. Chronology of complaints
A) onset:
ACUTE<6WK CHRONIC>6WK
Infectious arthritis
Crystal arthropathy
Reactive arthritis
Non inflammatory
arthritis(OA).
Inflammatory arthritis(RA)
Fibromyalgia
Causes of acute polyarthritis
• Infection Inflammation
• Gonococcal
• Meningococcal
• Lyme disease
• Rheumatic fever
• Bacterial endocarditis
• Viral (rubella, parvovirus,
Hep. B
• RA
• JRA
• SLE
• Reactive arthritis
• Psoriatic arthritis
• Polyarticular gout
• Sarcoid arthritis

7. B) Extent of articular involvement
Mono/Oligo2-5 jts Poly arthritis>5 jts
•Septic arthritis.
•Trauma.
•Crystal induced arthritis.
•Reactive arthritis.
•Juvenile rheumatoid arthritis.
•Psoriatic arthritis.
•Ischemic bone disease(AVN).
•Neoplasm-Villonodular
Synovitis.
•Monoarticular presentation of
ch. Arthritis.
•Charcot joint.
•Rheumatoid arthritis.
•Viral arthritis.
•Osteoarthritis .
•Psoriatic arthritis.
•Ankylosing spondylitis.
•Enteropathic arthritis.
•SLE
•Chronic gout.
•Chronic sarcoidosis.
•Polymyelgia rheumatica.
•Haemochromatosis.

8. C). Distribution of joint involvement
• Symmetrical:Rheumatoid
arthritis
small and large joints, upper and lower limbs.
Viral arthritis small and large joints; may be associated with rash and
prodromal illness; self-limiting.
Osteoarthritis targets , DIP and firstCMC joints in hands, knees, hips, back
and neck; associated with Heberden’s and Bouchard’s nodes.
SLE typically affecting small joints, clinical evidence of synovitis
Unusual, systemic findings.
JIA small and large joints, upper and lower limbs.
Polymyalgia
rheumatica
small and large joints, upper and lower limbs.
Chronic
sarcoidosis
small and large joints, upper and lower limbs.
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9. Asymmetrical joint involvement
Psoriatic arthritis targets PIP and DIP joints of hands and feet
(sausage appearance on examination), nail
pitting, large joints also affected.
Gout MTP great toe, in ch. Affects distal more than proximal
joints, history of acute attacks.
Ankylosing
spondylitis and
enteropathic arthritis
Tends to affect large joints, lower more than upper
limbs, possible history of inflammatory back pain.
Involvement of axial skeletal
AS, OA,RA(cervical spine only).

10. Rheumatic disease signs
• Swelling
• Pattern of joint
• Deformity
• Warmth
• Redness
• Tenderness
• Limitation of
joint
movement
• Crepitus
• Stability
• Function

11. History and physical examination
Is it articularTrauma/fracture
Soft tissue rheumatism
no
> 6 weeks
yes
Chronic
yes
Acute
Infectious arthritis
Crystal induced
Reactive arthritis
No
Signs of inflammation
Chronic
noninflamatory
arthritis
DIP, CMC1,Hip
,Knee joint
osteoarthritis
yes
Osteonecrosis
Charcots joint
no
yesChronic
inflammatory
arthritis
Joints involved
1-3
Psoriatic
Pauci JA symmetrical
>3
Psoriatic
Reactive
no
yes
PCP,MCP/MT
P
yes
Rheumatoid
no
SLE/Scleroderma
no

12. Rheumatoid Arthritis
• Commonest inflammatory joint disease seen in
clinical practice affecting approx 1%-3% of
population.
• Chronic multisystem disease of unknown cause.
• Characterized by persistent inflammatory synovitis
leading to cartilage damage, bone erosions, joint
deformity and disability.

13. Onset
• Although Rheumatoid arthritis may present at any
age, patients most commonly are first affected in the
third to sixth decades.
• Female: male 3:1
• Initial pattern of joint involvement could be:-
1) Polyarticular : most common
2) Oligo articular
3) Monoarticular
• Morning joint stiffness > 1 hour and easing with
physical activity is characteristic.
• Small joints of hand and feet are typically involved.

14. Pathogenesis of RA
• Strong associations between HLA-DR4(shared
epitope) and RA.
• HLA class II(APCs) surface antigens of immune
cells(B- lymphocytes, macrophages, dendritic cells).
• APC/T-cell interaction leads local inflammatory
response.
• Secretion of IL1,IL6,TNF, cytokines,PG leads to
synovitis.
• activation of osteoclast and chondrocytes-
>formation of inflammatory granulation tissue
named pannus->destruction of cartilage and bone-
>deformity of joint.

15. Pathology

16. Clinical manifestation
• Pre-clinical stage: muscle pain,tiredness,loss of
weight and generalized lack of well being.
• In early stage :
pictures of polysynovitis - pain, swelling, stiffness of
MCP,PIP joints then to wrist, feet, knee, shoulder.
Tenosynovitis –wrist extensors, finger flexors common
Morning stiffness >1hr.
 If Large joint involves: local warmth, synovial
hypertrophy,effusion,restrited movements.

17. In later stage
• Deformity become apparent.
• Acute pain of synovitis replaced by constant
ache pain of joint destruction.
• Joint instability and tendon rupture.
• Rheumatoid deformities.
• Restricted movements of joints.
• 1/3 rd patient pain and stiffness in cervical
spine.

18. Extra-articular features
• Constitutional symptoms ( most common)
• Rheumatoid nodules(30%)
• Hematological-
– normocytic normochromic anemia
– leucocytosis /leucopenia
– thrombocytosis
• Felty’s syndrome-
– Chronic nodular Rheumatoid Arthritis
– Spleenomegaly
– Neutropenia

19. Respiratory- pleural effusion, pneumonitis ,
pleuro-pulmonary nodules, ILD
CVS- pericarditis , pericardial effusion,
cardiomyopathy
Rheumatoid vasculitis-cutaneous ulceration,
digital gangrene, visceral infarction.
CNS- peripheral neuropathy, cord-
compression from atlantoaxial/midcervical
spine subluxation, entrapment
neuropathies
EYE- kerato cunjunctivitis sicca, episcleritis,
scleritis.

22. INVOLVEMENT OF JOINTS IN RA
• MCP 90-95%
• PIP 65-90%
• Wrist 80-90%
• MTP 50-90%
• Knee 60-80%
• Ankle 50-80%
• Shoulder 50-60%
• Hip 40-50%
• Cervical spine 40-50%
• Elbow 40-50%
• TM joint 20-30%

23. INVOLVEMENT OF JOINTS IN RA
• Don’t forget the
cervical spine
• Thoracolumbar,
sacroiliac, and DIP
joints of the hand are
NOT involved.

24. Deformities In RA
• Z deformity
• Swan neck deformity
• Boutonniere deformity

25. Laboratory investigations in RA
• CBC- TLC, DLC, Hb.
• Acute phase reactants.
• Rheumatoid Factor (RF).
• Anti- CCP antibodies.

26. Acute Phase Reactants
Positive acute phase reactants () Negative acute phase reactants ()
Mild elevations
– Ceruloplasmin
– Complement C3 & C4
Moderate elevations
– Haptoglobulin
– Fibrinogen (ESR)
– 1 – acid glycoprotein
– 1 – proteinase inhibitor
Marked elevations
– C-reactive protein (CRP)
– Serum amyloid A protein
– Albumin
– Transferrin

27. Rheumatoid Factor (RF)
• Antibodies that recognize Fc portion of IgG(70%).
• Can be IgM , IgG , IgA.
• clinical practice, IgM RF is usually measured(on
methodology).
• 85% of patients with RA over the first 2 years become
RF+.
• A negative RF may be repeated 4-6 monthly for the first
two year.
• PROGNISTIC VALUE-High titres of RF, tend to have
POOR PROGNOSIS, more extra articular manifestation.

28. Causes of positive test for RF
Rheumatoid arthritis(overall) 70%
Rheumatoid arthritis with nodules and extra-articular manifestations. 100%
Sjogrens syndrome 90%
Cryoglobulinemia 90%
Chronic liver disease 50%
Infective endocarditis 40%
SLE, Leprosy, Syphilis 30%
Tuberculosis 15%
Malignancy, Age>65 Yrs 20%
Normal Healthy People 5%

29. Anti Cyclic Citrullinated Peptide Antibodies
• peptidylarginine deiminase, an enzyme abundant in
inflamed synovium.
• IgG against synovial membrane peptides damaged via
inflammation.
• Anti-ccp Antibody have similar sensitivity to RF for RA
(70%) but much higher specificity (> 95%).
• Both diagnostic & prognostic value
• Predictive of Erosive Disease
– Disease severity
– Radiologic progression
– Poor functional outcomes

30. Test Sensitivity Specificity
Rheumatoid
factor
62% 85%
Anti-CCP 42% 98%
RF+Anti-CCP 33% 99.6%
SEROLGY IN RA:

31. Radiographic Features
• Peri-articular osteopenia
• Uniform symmetric joint space narrowing
• Marginal subchondral erosions
• Joint Subluxation
• Joint destruction
• Collapse
• Ultrasound detects early soft tissue lesions.
• MRI has greatest sensitivity to detect synovitis and
marrow changes.

34. Diagnostic Criteria's

35. ACR Criteria (1987)
1.Morning Stiffness ≥1 hour.
2.Arthritis of ≥ 3 joints observed by physician.
3.Arthritis of hand joints- PIP, MCP, wrist
4. Symmetric arthritis
5. Rheumatoid nodules
6. Positive Rheumatoid Factor
7. Radiographic Erosions or periarticular
osteopenia in hand or wrist joints
• Criteria 1-4 must be present for ≥6 wks
• Must have ≥4 criteria to meet diagnosis of RA

36. 2010 ACR/EULAR Classification Criteria
• a score of ≥6/10 is needed for classification of a patient as having definite RA
• A. Joint involvement SCORE
• 1 large joint 0
• 2−10 large joints 1
1−3 small joints (with or without involvement of large joints) 2
• 4−10 small joints (with or without involvement of large joints) 3
• >10 joints (at least 1 small joint)†† 5
• B. Serology (at least 1 test result is needed for classification)
• Negative RF and negative ACPA 0
• Low-positive RF or low-positive ACPA 2
• High-positive RF or high-positive ACP 3
• C. Acute-phase reactants (at least 1 test result is needed for classification)
• Normal CRP and normal ESR 0
• Abnormal CRP or normal ESR 1
• D. Duration of symptoms
• <6 weeks 0
• ≥6 weeks 1

37. Management

38. Goals of Therapy
• Control disease activity
• Alleviate pain
• Maintain function for essential
daily activities
• Maximize quality of life
• Slow progression/rate of joint
damage
• Prevent deformity

39. Treatment modalities for RA
NSAIDS
Steroids
DMARDs
Immunosuppressiv
e therapy
Biological
therapies
Surgery

40. NSAIDS
for symptom control
1) Reduce pain and swelling by inhibiting COX
2) Do not alter course of the disease.
3) Chronic use should be minimized.
4) Most common side effect related to GI tract.

41. Corticosteroids in RA
• Indications for systemic steroids are:-
1. For treatment of rheumatoid flares.
2. For extra-articular RA like rheumatoid vasculitis
and interstitial lung disease.
3. As bridge therapy for 6-8 weeks before the
action of DMARDs begin.
4. Maintenance dose of 10mg or less of
Prednisolone daily in patients with active RA.
5. Sometimes in pregnancy when other DMARDs
cannot be used.

42. Disease Modifying Anti-rheumatic Agents
• Drugs that actually alter the disease course .
• Should be used as soon as diagnosis is
made.
• Appearance of benefit delayed for weeks to
months.
• NSAIDS must be continued with them until
true remission is achieved .
• Induction of true remission is unusual .

43. DMARDs
NAME DOSE SIDE EFFECTS MONITORING ONSET OF
ACTION
1) Hydroxycloro
quine
200mg twice
daily x 3 months,
then once daily
Skin
pigmentation ,
retinopathy
,nausea,
psychosis,
Myopathy
Fundoscopy&
perimetry yearly
2-4 months
2) Methotrexate 7.5-25 mg once a
week orally/c or
i/m
GI upset,
hepatotoxicity,
Bone marrow
suppression,
pulmonary
fibrosis,teratogen
ic.
Blood counts,LFT
6-8 weekly, Chest
x-ray annually,
urea/creatinine 3
monthly;
Liver biopsy
1-2 months

44. NAME DOSE SIDE EFFECTS MONITORING ONSET OF
ACTION
3)Sulphasalazine 2gm daily p.o Rash,
myelosuppression, may
reduce sperm count
Blood counts ,LFT
6-8 weekly
1-2
months
4)Leflunomide Loading 100 mg
daily x 3 days,
then 10-20 mg
daily p.o
Nausea,diarrhoea,alope
cia, hepatotoxicity
LFT 6-8 weekly 1-2
months
zine

45. When & what DMARDs
• Rheumatologists start DMARDs from Day
1.
• METHOTREXATE is the DMARD of choice,
most widely prescribed in the world.
• DMARD combination is specially effective
if they include Methotrexate as an anchor
drug.

46. Limitations of conventional DMARDs
1) The onset of action takes several months.
2) The remission induced in many cases is partial.
3) There may be substantial toxicity which
requires careful monitoring.
4) DMARDs have a tendency to lose effectiveness
with time-(slip out).
 These drawbacks have made researchers look
for alternative treatment strategies for RA- The
Biologic Response Modifiers.

47. BIOLOGICS IN RA
• Cytokines such as TNF-α ,IL-1,IL-10 etc. are key
mediators of immune function in RA and have
been major targets of therapeutic manipulations in
RA.
• Various biological approved in RA are:-
1) Anti TNF agents : Infliximab Etanercept Adalimumab
2) IL-1 receptor antagonist : Anakinra
3) IL-6 receptor antagonist : Tocilizumab
4) Anti CD20 antibody : Rituximab
5) T cell co stimulatory inhibitor : Abatacept

48. How to monitor Tt in RA?
• Disease activity is assesed by several parameters…
duration of morning stiffness, tender joint count,
swollen joint count, observer global assessment,
patient global assessment, visual analogue scale for
pain, health assessment questionnaire,ESR,NSAID
pill count,DAS score etc..
• Patient on MTX,SSZ or leflunamide show clinical
improvement in 6-8 wks.
• Patient should be observed for 6 months before
declaring a DMARD ineffective.

49. 2012 ACR Update

50. Surgical Approaches
• Increases function
of the joint
• Decreases pain
and inflammation
• Beneficial as an
early treatment
option
• Not a cure!
Synovectomy

51. Total Joint Arthroplasty&Arthroscopy

52. Arthrodesis
Limited
joint motion
Pain
reduction

53. Seronegative
spondyloarthropathies
1. Ankylosing spondylitis (the
prototype)
2. Psoriatic arthritis
3. Reactive arthritis
(Formerly called Reiter’s syndrome)
4. Enteropathic arthritis
5. Undifferentiated
spondyloarthropathies
Mnemonic is PURE-A

54. Why grouped
1. HLA-B27 association
2. Enthesitis
3. Axial skeleton arthritis
1. Spondylitis (inflammation of vertebral bodies)
2. Sacroiliitis (inflammation of sacroiliac joint)
4. Peripheral arthritis
1. Asymmetric (cf rheumatoid arthritis)
5. Extraärticular manifestations
6. Seronegativity
– Rheumatoid factor and ANA negative

55. HLA-B27 association
• Ankylosing spondylitis: 95%.
• Reactive arthritis: 70%
• Enteropathic arthritis: 50%
• Psoriatic arthritis: 35%

56. Ankylosing Spondylitis
• AS is a chronic, progressive immune-mediated
inflammatory disorder that results in ankylosis
of the vertebral column and sacroiliac joints.
• Complete fusion results in a complete rigidity
of the spine, a condition known as bamboo
spine.

57. Cont…
• Over time, joints in
the spine can fuse
together and cause a
fixed, bent-forward
posture.
• HLA-B27 gene is
associated with AS.
• Age of onset typically
between 15 and 35
years.
• M:F= 3:1

58. Age at Onset Distribution of AS and
Rheumatoid Arthritis (RA)

59. Pathogenesis
• HLA-B27 genotype.
-90% of
patients
>Tumor necrosis
factor-alpha (TNF α)
>IL-1,IL6,

60. CONT..
• Continued inflammation
of the:
-ligaments,
-tendons,
-joint capsules (soft
tissues surrounding the
joint),
-and joints of the spine -
cause the spine to fuse
together (ankylose) as the
joints and disc spaces are
replaced by bone.

61. Clinical features
• Axial manifestations:
 Chronic low back pain, With or without buttock pain.
 Morning stiffness, relief with activity.
 Limited axial motion.
 Axial deformity.
• Extra skeletal manifestations:
Anorexia,malaise,weight loss,fatigue,low fever,
Difficulty in respiration.
Iridocyclitis
Vasculitis.

62. Peripheral manifestations
Enthesitis Peripheral arthritis Dactylitis
AS: Signs and Symptoms
50% patients with
enthesitis
Up to 58% patients
ever had arthritis
Much smaller number
of patients

63. Investigations:
• a blood test for the HLA-
B27 gene.
• X-ray
-which show
characteristic spinal
changes and Sacroiliitis.
• tomography and magnetic
resonance imaging of the
sacroiliac joints.

64. Diagnostic criteria
• THE ROME CRITERIA (1963)
• THE NEW YORK CRITERIA (1968)

65. THE ROME CRITERIA
according to this ,as is diagnosed if b/l Sacroiliitis
is seen along with one of the following.
a) LBA & stiffness of 3 months duration not
relieved by rest
b) pain and stiffness in the thoracic spine
c) limited lumbar spinal movement
d) limited chest expansion
e) history or evidence of iritis or its sequelae

66. THE NEW YORK CRITERIA
• Clinical components:
1. Low back pain and stiffness > 3 months,
not relieved by rest.
2. Limitation of motion of the lumbar spine
in 3 planes.
3. Limitation of chest expansion(<2.5cm)
• Radiological component:
– Sacroiliitis Grade >2 bilaterally or Grade 3-
4 unilaterally

67. Radiological Criteria Based On Sacroiliac Joint
Radiographs
(Definite AS= radiological criterion + one clinical criterion)
Gr 0 : Normal.
Gr 1: Possibly
Normal(minimal
Sclerosis).
Gr 2: Definite
Marginal Sclerosis.
Gr 3: Definite
Erosion And
Sclerosis.
Gr 4: Complete
Obliteration And
Ankylosis.

68. Treatment
• No cure is known for AS!
• treatments and medications are available to
reduce symptoms and pain.
• three major types of medications used.
NSAIDS.
DMARDS.
Immunosuppressive.
TNF blockers: infliximab,atenarcept etc.

69. Surgical Management:
• may include OSTEOTOMY for marked deformities
of the hip/spine.
• occasionally, hip or knee ARTHROPLASTY is used.
- if there is severe arthritis of those joints.
Nursing Responsibilities:
• Baseline ROM and chest expansion exercise.
• proper positioning at rest is essential.
• the mattress should be firm, and pillows must be
avoided.

70. •SWIMMING
•BADMINTON
•JOGGING
•YOGA
•DEEP BREATHING
EXERCISES
•PRONE LYING
•MODIFICATION OF
WORK

71. Reactive Arthritis/Reiter”s Syndrome
• Reactive arthritis or Reiter’s syndrome is a
acute,painful,asymmetrical form of inflammatory
arthritis that develops in reaction to an infection
by bacteria or virus.
• a triad of nongonococcal urethritis, conjunctivitis, and
arthritis.
• RF-seronegative, HLA-B27-linked arthritis.
• The arthritis may be “Additive or Migratory.”

72. Causes/pathogenesis
• Streptococcal throat infection.
• glandular fever.
• viral flu.
• food poisoning.
• sexually acquired

73. Signs and symptoms
• Dysuria,an increased frequency of urination.
• Prostatitis,cervicitis, salpingitis,vulvovaginitis
• penile lesions called balanitis circinata.
• inflammation of the eyes in the form of
conjunctivitis or uveitis

74. •Swelling, pain in large joint, knee etc
•Keratoderma blennorrhagica
•Palms/soles
•Oral ulcers (usually shallow and painless)
•Inflammatory back pain (50% of patients)
•Enthesitis (40%)
•Dactylitis (40%)

75. Treatment
• The main goal of treatment is to identify and
eradicate the underlying infectious source with
the appropriate antibiotics if still present.
• Otherwise, treatment is symptomatic for each
problem.
• Analgesics particularly NSAIDs, sulfasalazine,
steroids .
• immunosuppressants may be needed for
patients with severe reactive symptoms that do
not respond to any other treatment.

76. Psoriatic arthritis
• A chronic inflammatory arthritis in association with skin
psoriasis(7%-45%).
• Characterized by osteolysis and bony proliferation.
• Males and females are equally affected.
• Range from mild nondestructive disease to a severely rapid
and destructive arthropathy.
• HLA B27 associated & Seronegative.
• Characterized by synovitis, Enthesitis, dactylitis, spondylitis,
skin and nail psoriasis.

77. Moll And Wright Clinical Pattern
• Including 5 clinical patterns:
Asymmetric mono-/oligoarthritis (~30% [range 12-
70%])
Symmetric polyarthritis (~45% [range 15-65%])
Distal interphalyngeal (DIP) joint involvement (~5%)
Axial (spondylitis and Sacroiliitis) (HLA-B27) (~5%)
Arthritis Mutilans (<5%).

78. Moll And Wright Clinical Pattern
• Including 5 clinical patterns:
Asymmetric mono-/oligoarthritis (~30% [range 12-
70%])
Symmetric polyarthritis (~45% [range 15-65%])
Distal interphalyngeal (DIP) joint involvement (~5%)
Axial (spondylitis and Sacroiliitis) (HLA-B27) (~5%)
Arthritis Mutilans (<5%).
Nail/skin change- 90%

80. Opera glass hand

82. CASPAR Criteria For Diagnosis
• Inflammatory articular disease (joint, spine, or
entheseal)
• With 3 points from following categories:
 Psoriasis: current, history, family history.
 Nail dystrophy.
 Negative rheumatoid factor.
 Dactylitis: current, history.
 Radiographs:(hand/foot) evidence of
osteolysis, juxta-articular new bone
formation(pencil in cup).
• Specificity 98.7%, Sensitivity 91.4%

83. Treatment of PSA

85. Enteropathic Arthritis
• Affects 10-20% of patients with
inflammatory bowel disease (IBD)
• Peripheral arthritis affects 10-20% of IBD
patients
– Generally affects knees, ankles, and feet
– Always indicates active IBD
• Radiographic axial arthritis affects 10% of
IBD patients
– Frequently asymptomatic
– Independent of bowel inflammation

86. Treatment
• Nonsteroidal antiinflammatory agents
– Indamethacin
• Disease modifying anti-rheumatic drugs
(DMARDs)
– Methotrexate: inhibits recruitment of CD4 and
CD8 T cells
• Tumor necrosis factor antagonists
– Infliximab: a monoclonal antibody that binds to
TNF and inhibits binding of TNF to its receptor
– Etanercept: similar emchanism to infliximab
• For axial arthritis, exercises to maintain
posture and flexibility

87. Systemic erythematosus Lupus
• Immune complex deposition disease, involving
many organs.
• Arthritis: Nonserosive 2 or > joints
• Female:Male 10:1
• ANA and other criterion will make the diagnosis.
• AVN is the complication.