About The Author Dr Manoj R.

kandoi is the founder president of Institute of Arthritis Care & Prevention an NGO involved in the field of patient education regarding arthritis. Besides providing literature to patient & conducting symposiums, the institute is also engaged in creating patients Self Help Group at every district level. The institute also conducts a certificate course for healthcare professionals & provide fellowship to experts in the field of arthritis. The author has many publications to his credit in various journals. He has also written a book The Basics Of Arthritis for healthcare professionals. The author can be contacted at: Dr manoj R. kandoi C-202/203 Navare Arcade Shiv Mandir Road, Opposite Dena Bank Shiv mandir Road, Opposite Dena bank Shivaji Chawk, Ambarnath(E) Dist: Thane Pin:421501 State: Maharashtra Ph: (0251)2602404 Country: India Membership Application forms of the IACR for patients & healthcare professionals can be obtained from. Institute of Arthritis Care & Prevention C/o Ashirwad Hospital Almas mension, SVP Road, New Colony, Ambarnath(W) Pin:421501 Dist: Thane State: Maharashtra Country: India Ph: (0251) 2681457 Fax: (0251)2680020 Mobile ;9822031683 Email: drkandoi@yahoo.co.in Preface: Studies have shown that people who are well informed & participate actively in their own care experience less pain & make fewer visits to the doctor than do other people with arthritis. Unfortunately in India & many third world countries we do not have patient education & arthritis self management programs as well as support groups. This is an attempt to give a brief account of various arthritis, their prevention & self management methods which can serve as useful guide to the patients of arthritis. It would be gratifying if the sufferers of the disease knew most of what is given in the book. Acknowledgement\ I am thankful to Dr (Mrs) Sangita Kandoi for her immense help in proofreading & for her invaluable suggestions. The help rendered by Nisha Jaiswal is probably unrivalled. Thanks also to vidya, sheetal and parvati for their continous support throughout the making of the book. The author is grateful to his family for the constant inspiration they offered. The author alone is responsible for the shortcoming in this piece of work. He welcomes suggestions for improvement from the readers.

Neuropathic Arthritis:
Introduction: Arthritis caused by repeated minor injuries to the joint which is insensitive to pain leading to its disorganisation is known as neuropathic arthritis. It is named after JeonMartin Charcot (1825-1893) who first described it in association with tabes dorsalis. Disorders associated with charcot's joint: - Diabetes mellitus - Syringomyelia - Syphilic - Spine bifida - Chronic alcoholism - Meningomyelocele - Hansens disease - Congenital insensitivity to pain - Peripheral nerve injuries - Amyloid neuropathy - Charcot -marie -tooth disease Etiopathogenesis: Reduction in joint sensibility Protective function of pain is lost Loss of protective muscle reflex Harmful joint strain go unprevented Cumulative strains leading to severe degenerative changes Articular cartilage and subchondral bone worn away. ligament laxity and joint instability. Types of charcots joints: 1. Atrophic: "Pencil -in -cup" deformation, resorption of bone end, usually affects upper extremities. 2. Hypertrophic: Joint space narrowing, with bony sclerosis, new periosteal bone formation, articular surface fragmentation and joint subluxation can be seen. Stages in formation of charcots joint: Stage I: Joint subluxation, osteoporosis, cortical defects. Stage II: Osteolysis, fracture, periosteal elevation or new subperiosteal bone formation. Stage III: Healing stage, reconstructive, decrease swelling and bony ankylosis. Clinical features: Knee, ankle and subtalar joints are most commonly affected in the lower limb and elbow in upper limits. Joints in the spine may also be affected.

Symptoms: Common presenting complaint is painless swelling and instability of joint. Signs: Irregular hypertrophy at the bone ends Moderate restriction of movements ~ Ligament laxity with excessive side to side movements Localized erythema, swelling and increased skin temperature can also be noted.

Associated findings in charcot's joints: In tabes dorsalis, the lower extremities and spine are commonly involved. Other signs include ataxia, argyll robertson pupils, absent knee reflexes and, absent deep position, vibration and pain sense. In Syringomyelia upper extremities are commonly involved. Clinically features of sensory dissociation, loss of pain and temperature, and preservation of touch is noted. Deep sensation is undisturbed. Progressive muscle atrophy in the arms and fibrillation and trophic changes in the fingers may also be noted. Radiographic changes: Exaggerated changes of degenerative arthritis seen such as loss of cartilage space, absorption of bone ends, hypertrophy of bone at the joints margins etc. Subluxation or dislocation may be noted. Treatment: Protocol

Conservative - Supportive and protective bracing - Role of biphosphate pamidronate under investigation.

Surgicals - Surgical fusion in corrective position can be obtained.

Criteria for surgical intervenation: Instability of the foot or ankle Deformity Chronic ulceration Progressive joint destruction (despite conservative care) Adequate circulation No active infection Systemic factor: Patient should be medically stable and compliant and have the potential for returning to an active lifestyle

Surgical methods used: Joint involved Knee Methods used - Straight caliper with an ischial fitting ring - Surgical arthrodesis using charnleys compression appartus - Ankle corset - Arthrodesis - Special shoes with steel arch supports plus a cane - Surgical arthrodesis is usually not practical - Subtrochantric shanz osteotomy with 30 of abduction. - Corset - Spine fusion - Hinged elbow support providing lateral stability

Ankle Foot

Hip Spine Elbow

Timing of surgical reconstruction / management: It should be done when stage of reconstruction begins i.e. when acute inflammatory condition has subsided & there is radiographic evidence of healing. Patterns of bone & joint involvement in neuropathic diabetes: 1. Forefoot: Radiographic findings are often atrophic & destructive mimicking osteomyelitis. Plantar ulceration is an associated findings. 2. Tarsometatarsal joints: Characterized by disruption of the TMT joints often with collapse of the midfoot. Plantar ulceration frequently develops at the apex of the collapsed cuneiform or cuboid. 3. Naviculocuneiform, talonavicular & calcaneocuboid joints: There is usually dislocation of the navicular or disintigeration of naviculocuneiform joints. 4. Ankle joint: Infrequent but associated with severe deformity & instability. It may also be associated with involvement of subtalar joint. 5. Calcaneus: It is characterized by rare avulsion fracture of the posterior process of the calcaneus. Factors responsible for noninfective bone & joint destruction in diabetic foot: Peripheral neuropathy with loss of protective sensation Autonomic neuropathy with increased peripheral blood flow Mechanical stress of weight bearing , Repititive trauma Nonenzymatic glycosylation of collagen Decrease cartilage growth activity Corticosteroid -induced osteoporosis

Acute Charcots joint in diabetes - Absent Deep Tendon reflex - Decreased vibratory sense - Loss of protection sensation - Fever - WBC Count - Shift in differential WBC Count - ESR - Indium-III Scans - MRI - Bone Biopsy + + + Normal / Normal Differentiates between two

Osteomyelitis in diabetes + Raised +