SANDHI VATA

SANDHIGATVATA VIS-À-VIS OSTEOARTHRITIS

Disease Sandhigatvata is described first by Charaka in the

name of “Sandhigat Anila” with symptoms of Shotha,

palpation feels as bag filled with air, Shula on Prasarana and

Akunchana (pain on flexion and extension of the joints) (Ch. Chi.

28/37).

Sushruta also mentioned Shula and Shotha in this disease

leading to the diminution (Hanti) of the movement at joint

involved (Su. Ni. 1/28, 29). Another disease Vatakantaka is

mentioned by Sushruta which occurs due to the vitiated Vata by

involving Khuda Sandhi.

According to Dalhana and Gayadasa,Khadu means Padjangha Sandhi i.e. ankle (Su. Ni. 1/79). The

other view has been quoted according to which Khadu may be

taken as Parshani (calcaneum).

 

Madhavakara has not explained Shotha but mentioned

Atopa as a symptoms of Sandhigat Vata (M. Ni. 22/21), which

may also be taken equivalent to air filled bag. He has added one

more symptom i.e. Hanti Sandhi (restricted flexion and

extension).

Thus, the disease Sandhigatvata can be defined as a joint disease with symptom of Shula, which aggravates by movement,

Shotha with complete restricted movements at later stages. This

disease is comparable with Osteoarthritis, a degenerative joint

disease, the symptoms of which are same as Sandhigatvata and

usually occurs after the age of 40 years.

ETYMOLOGY OF SANDHI

The word Sandhigatvata is comprised of two words viz. Sandhi

and Vata. Sandhi is an anatomical part and Vata is a physiological

aspect in the body.

Sandhi or joints merely meeting places of two or

more bones with one other, which are essential to motor function

of the skeleton.

Classification : (Structure)

Locomotion is made possible by the presence of joints in

the body. Affliction of Sandhi is central event in the Samprapti of

Sandhigatvata. It is reckoned to be the Upadhatu of Medodhatu. The

function of the Sandhi is sustained by Sleshaka Kapah and Snayu

the forms imparts lubrication to be the joint and the later brings

about stability.

Acharya Sushruta has explained the joints and their classification in

a fine manner which are as follows.

Primarily Sandhi can be divided into two groups :

A) Sthira Sandhi (Fixed Joints)

B) Cheshtavaha Sandhi (Mobile Joints)

Cheshtavaha Sandhi :

 it has further being divided into two

types.

i) Bahu Cheshta (Synovial joints)

ii) Alpa Cheshta (Cartilagenous joints)

 Dosha : According to Ayurvedic classics all their functions are

controlled by Doshas . In Sandi following Doshas can be

described.

a) Vata : Vyana Vayu is stated to be located in Hridaya and

to be circulated in all over the body doing the functions

of movements of all types. (Su. Ni. 1/17-18).

b) Kapha : Sleshaka Kapha is located by the support of

Sleshmadhar Kala in Sandhis and lubricates the Sandhis

to perform the movement in the normal direction. (Su.

Su. 21/14).

iv) Physiology of Sandhi : The physiological functions of the

Sandhi include Akunchana, Prasarana, Utkshepana,

Avakshepana, etc. as explained by Acharyas in their classics

(Su. Ni. 1/17-18; Dh. And Su. Ni. 1/13 Gy.).

  VATA

After the general description, regarding Sandhi now it is

important to discuss Vata the another responsible factor for the

disease Sandhivata.

RELATION BETWEEN VATA AND SANDHI

There is a relation between the Dosha and Dushya because

of their Bhautika constitution, which has been well narrated in

Ashtanga Hridaya while describing the properties, actions and

importance of three Doshas. This is also called as Ashaya

Ashrayai Bhava i.e. inter-relation between Dosha and Dushya. It

has been eluded that Vata is located in Asthi, Pitta is in Sweda

and Rakta and Kapha in Rasa, Mamsa, Meda, Majja and Shukra. It

is because of this relation that the drugs or dietetic regimens

which augment the one Dosha, also have the effect on their

dependant Dhatu. By augmentation of the Dosha, there would be

similar effect on their respective Dhatus. But, contrary to this

augmentation of Vata (Ashrayi), due to its properties will lead to

decrease (Kshaya) in the Asthi (Ashraya) and vice versa. In the

similar way it is related with Kapha. Kshaya of Kapha will cause

increase in the quantum of Vata and vice versa (Su. Su. 15/7; A.

H. Su. 11/26-28).

DEFINITION OF SANDHIGATAVATA

There is no clear-cut definition of Sandhigatavata, but however

the classical text of Ayurveda, the Charaka Samhita reveals that

after Nidana Sevana aggravated Vata enters in the Sandhi and get

established thereby producing swelling of the joints, which is felt

like a bag filled with air and the pain occurs mainly during the

flexion and extension the movements of the joints.

SYNONYMS

Different authors named this disease according their own

views, but most of them are out of views. The probable synonyms

of Sandhigatvata used in the different context or considered by the

commentators equivalent to Sandhigatvata are as follows.

Sandhigata Anila (Charaka)

Sandhigata Vata (Sushruta)

Khudavata (Charaka)

Gulphavata (Chakrapani)

Vatakhuddata (Charaka)

Vatakantaka (Sushruta)

Kaluka (Charaka)

INCIDENCE OF SANDHIGATVATA

The incidence of Sandhigat Vata, may vary according to Dosha,

Vaya, Linga etc. the detailed study of these factors are as follow :

1) Dosha : For the Prakopa of Vata, both Ushna and Sheeta Guna

are necessary with Ruksha Guna i.e. when the Rukshadi Guna

gets contact with Ushna, Chaya occurs. When the same

combiners with Sheeta, Prakopa of Vata occurs (A. H. Su.

12/19-20).

 So any Dosha with dry whether and having both

extreme hot or cold climate are more prone to this disease.

2) Vaya : As a natural course, Vata becomes predominant in body

during old age and naturally the persons of these age group

have more Vatika disorders. So, between the age of 40 and 65

years, it is a common disorder.

3) Linga : There is no specific description of Vata Vyadhi or

Sandhivata according to sex i.e. male or female in present

Ayurvedic text. That means the role of Linga (sex) in

Sandhivata is not classified. But according to modern science,

usually females are suffering from Sandhigatvata more than men.

CLASSIFICATION OF SANDHIVATA

It can be classified in different ways as there is no

classification is mentioned in our texts available.

A) According to pathogenesis of Vata it can be classified as

below.

i) Dhatukshayajanya: Kshaya of Dhatus is the main cause

Of vatavyadhi.reson behind this is kshaya create laghu, ruksha etc guna in body that make body more prone to be diseased by elevated vata dosh.

ii) Avaranajanya: The primary cause of Avarana of Srotasa by Kapha or Meda. Avarana create obstruction in body system like digestive, circulatory, respiatoy, nervous system etc.

so, due lake of nutrition of further dhatu Kshaya is occure. And body prone to be diseased by elevated vata dosh.

Shloka…

iii) Both: Kshaya as well as Avaranajanya.

B) According to Nija and Agantuja, it can be classified in two

varieties.

i)   Nija Sandigatavata  it is due to vata elevating diet, ruteen, lake of proper nutrition, weak digestive power and all internal facters that makes  body prone to be diseased. in short if sandhigatavata is due to vitiated doshas that is called nija sandhigatavata.

   ii) Agantuja Sandhigatavata if sandhigatavata is due to external factors like trauma, shastra kriya (joint operative), shortening of one leg, sandhigatavata of one leg increase the probability of sandhigatavata of   another leg.

NIDANAPANCHAKA OF SANDHIVATA

The knowledge of disease is obtained by the study of

Nidana, Purvarupa, Rupa, Upashaya, Samprapti which are termed

as Nidana Panchaka.

Ayurvedic literature does not reveal the special etiological

factor for Sandhivata however, the aggravative factors for vata

can be adopted for it, Vata particularly Vyana vayu has a close

relationship with the movement of Sandhi, so, its aggravative

factors which can be produce Sandhivata are as follows.(Cha. Chi.

28/14-22)

Aharaja :- Ruksha - Laghu – Visthambhi - Sheeta – Katu – Tikta

- Kashaya Annasevena, Sheetapana, Adhyasana, Viruddha –

Asatmya – Pramita – Mithya Ahara etc.

Viharaja :- Ati Vata – Atapa sevana, Ati Plavana, - Vyayama –

Vyavay – Chesta, Vegavidharana, Ratrijagarana, Divaswapa,

Marmaghata, Abhighata etc.

Manasaja :- Chinta, Krodha, Shoka, Bhaya etc.

Kalaja :- Abhra (cloudy season), Aparahna (evening), Aparatra

(end of night), Sheetakala (winter), Varsha (rainy season) etc.

Other than these, the factors which can produce Avarana of

Kapha or Meda and the factors which make Dhatukshaya also

cause Sandhigatvata.

 Asthi being a prime seat of vata, as well as

important part of sandhi. Its Kshaya can produce aggravation of

vata and Kha-vaigunya in Sandhisthana, leading to Sandhivata.

Medovriddhi can also produce Sandhivata, because of

sthaulya weight-bearing joints have over burden and may lead to

Sandhivata.

PURVARUPA

The Purvarupa manifests in the Sthanasanshraya stage of

Shadkriyakala. Charaka has quoted that Avyakta Lakshanas of

Vata Vyadhi are to be taken as its purvarupa. Commentator

Vijayrakshitji explains the term Avyakta as the symptoms which

are not manifested clearly. Hence, mild or occasionall

Sandhishula, meda dhatu kshaya prior to manifestation of disease Sandhivata may be taken as Purvarupa.

RUPA

The symptoms which demonstrate a manifested disease are

included under Rupa. A clear understanding of Rupa is inevitable

for accurate diagnosis (M. Ni. 3/7).

In Sandhigatvata the main cardinal symptoms are mentioned

which are common for all joints.

Madhavakara has given another symptom Atopa. The

meaning of word Atopa can be taken as Shotha or

Sandhisphutana.

These main symptoms are as follow:

1) Sandhishula : Shula is a main symptom in Sandhivata. Pain

usually increases by movements likeAkunchana, Prasarana

because of vata prakopa. It also said to be worst towards

evening because of the tendency of vata which naturally

aggravates at evening period, hence the pain.

2) Sandhishotha : Vatapurna druti sparsh type of Shotha has been

described by all Acharyas. Srotorodha occurs due to vata Sanga

which is responsible for shotha. Being a vatic type, on

palpation the swelling is felt like a bag filled with air but

Madhavakara gave this term a new name of Atopa (M. Ni.

22/21).

3) Sandhihanti : Charaka has mentioned this symptom as a

painful prasarana – akunchana Pravritti. First sushruta

explained this symptom followed by Madhavakara. This word is

explained by Dalhana and Gayadasha as inability to flexion and

extension. However this symptom may not be seen in early

stages. When the disease aggravated the vitiated vata may

produce Stambha and there inability of movements.

4) Sandhisphutana : Sandhigatavata is localized vata vyadhi in which

prakupita vayu affects Sandhi. This Sthanasamsraya is result

of srotoriktata present at sandhi. That means Akash

Mahabhuta is increased at the site of sandhi and Shabda is a

guna of Akash. Hence, in the process of extension and flexion,

Shabda is heard or palpated.

UPASHAYA

All drugs, diet, regimen and kal which give relief in

Sandhigatavata may be taken as Upashaya. For example Abhyanga,

Swedana, Ushna Ahara, Ushna Ritu etc.

ANUPASHAYA

All drugs, diet and regimen which exaggerate the disease

are taken Anupashaya for that disease. Also Hetus of that disease

can also be taken as Anupashaya. The diet having Laghu, Ruksha,

Sheeta Gunas, Anasana, Alpasana, Sheeta Ritu, evening time can

be considered as Anupashaya as they increase pain.

SAMPRAPTI OF SANDHIVATA (PATHOGENESIS) :

Samprapti means the course of a disease right from the

affliction by the causative factors up to its manifestation.

Samprapti is that process extending from Nidana Sevana to

Vyadhi Vyaktavastha. The genesis of the disease by the specific

action of vitiated Doshas responsible is causation called

Samprapti (Ch. Ni. 1/11). Due to Nidana Sevana, the Vata gets

Prakupita which gets accumulated in Rikta Srotasa leading to the

various generalized and localized disease of Vata (Ch. Chi. 28/18-

19).

Sandhivata has no specific Samprapti as per the texts

available. It is classified under the heading of the Vata Vyadhi. It

is also a type of Vata Vikara, where the Dushita Vata involves the

Sandhi and hence, the nomenclature – Sandhivata. Here

Sandhivata is categorized as a localized disease of Sandhi as it is

the disease of Sandhi due to Vata Prakopa, so it can be derived

that all factors contributing to the aggravation of Vata Dosha in

the body are liable to produce the disease Sandhivata. In

Sandhivata early pathology starts with Vata specially Vyana Vayu,

which is aggravated by different factors and takes it up to the

Prasara stage.

 The Kha-vaigunya of Sandhi leads its Sthanasanshraya.

 The Prakopa of Vata may be due to two causes

i.e. 1) Avarana and 2) Dhatukshaya.

 In the obese persons,

Sandhivata is commonly seen. It may be due to Avarana of Kapha

and Meda.

Sandhivata being a Degenerative disease and mainly

occurring in the old age may also be considered due to the pure

Dhatukshaya. In such type of disorders Charaka mentioned that

the Kha-vaigunya is mainly due to empty Srotasa (Ch. Chi.

28/18).

 According to Chakrapani this means the diminution of

Sleshaka Kapha specially its Sneha guna in the joint involved.

In other words, the vata Dosha is aggravated due to

different factors and Vata flows out of its Ashaya to circulate in

the entire body and its constituents.

 During circulation it gets localized in the roots of Majjavaha Srotasa, i.e. Asthisandhi.

 In the Majjavaha Srotasa the Khavaigunya may already present.

Because unless there is Khavaigunya of Srotasa the Dosha will

note take Ashraya. The chief qualities of vata are – Khara,

Ruksha, Vishad and Laghu. Sandhi gives Ashraya to Sleshaka

Kapha which has to following qualities Guru, Snigdha, and Mrudu.

When aggravated vata gets localized in the Sandhi, it over powers

Kapha as well adversely affects on its qualities.

The chief task of the Kapha is to sustain or Dharana. This chief aim of Kapha is destroyed by the influence of aggravated Vata.

 When aggravated Vata is localized into single joint the disease will be reflected only in one joint, but if Vata is present in two or more joints the

disease will be represented by multiple joints involvement.

The disease Sandhigatvata occurs when the patients attains

Vatika phase of life, say after 50 years of age. As in this period

Vata Dosha is found predominant due to Dhatuhani, consequently

Vatika disorders are more evident. Hence, it can be said that as

this entity itself is a degenerative joint disease on the other

hand, the diet regimen which is mainly dominated by Vatika

qualities say, Vata Vardhaka Ahara Vihara can be envisaged as the

predisposing factors in Sandhivata. Due to all days i.e. Kalaja

Nidana, it causes Ashtivaha Srotodushti and Kha-vaigunya in

joints, with Vata Vardhaka Ahara Vihara, it leads to Vata

Sanchaya and Agnivaishamya. Further Agnivaishamya cause

Anuloma Dhatukshaya which ultimately results in Vata Prakopa

and vice versa. Because of Anuloma Dhatukshaya the vitiated

Vata moves in the body and settles down in joints.

Here a very pertinent question arises why the vitiated Vata

settles down only in joints ? The most ameliorate answer to this

question is that there is inter-relationship between the Dosha and

Dushya which is called Ashraya-Ashrayi Bhava Sambandha. Due

to this relation only the drugs and dietetic regimens which

augment the one Dosha also have the effect on their host Dhatu.

While commenting on Sushruta Samhita, the Gayadasa quoted

the wording of an unknown author “Though the Vyana Vayu is

functioning all over the body but its main site of action is

Sandhis” (Su. Ni. 1/130 - Gayadas). It has also been stated that as

Vata is mobile in nature so a particular seat can not be attributed

to it and the sites which are more mobile can be considered as a

site of Vyana Vayu. Hence, if we considered the seat of Vyana

Vayu as Sandhi obviously Vyana Vayu may have close relation

with Sleshaka Kapha because Sandhi is Upadhatu of Meda and

Meda is Ashraya of Kapha Dosha thus, there is inter-relation

between them.

Whenever, the Vyana Vayu gets vitiated than

simultaneously Some Sthana Vikriti or Kha-vaigunya at joints

may takes place. Because of this Kha-vaigunya at Sandhis, the

vitiated Vyana Vayu settles down in joints and causes Asthi

Srotodushti, which results in Asthigata Vata and Sandhigata Vata

(Ch. Chi. 28/18). Both Asthigata and Sandnhigata Vata

combinedly cause the symptom Sandhi Shula and Sandhi Shotha.

Sandhistha Vata separately causes Sleshaka Kaphakahsya due to

Ruksha and Khara Guna. Here the Ruksha and Khara Guna of

Vata are considered as antagonizing for Sleshaka Kapha which

eventually results in diminution of Sleshaka Kapha (synovial

fluid). Due to this diminution of Sleshaka Kapha by Sandhistha

Vata, the symptom Akunchana Prasaranajanya Vedana at joints

takes place. Excessive accumulation of Vata at Sandhi by

Sandhistha Vata can cause Vatapurna Dritivata Shotha.

Thus, we can say collectively the Asthigata Vata,

Sandhistha Vata, Meda and Kaphavrita Vata and Sleshaka

Kaphakshaya leads to a pathological condition called Sandhivata.

Realizing of importance of Samprapti, Acharya Charaka has

dealt in detail the various aspect of Samprapti by classifying it in

following six types (Ch. Ni. 1/11).

1) Sankhya Samprapti : Sandhivata is in numbered one only as no

other variety is mentioned in texts.

2) Pradhanya Samprapti : From the view point of Doshika status

in Sandhivata, Vata is Pradhanatam in all the three Doshas.

3) Vidhi Samprapti : Sandhivata is Nija, Vataja and in general is

difficult to cure.

4) Vikalpa Samprapti : Sandhivata being Vatavyahi are get the

increased Vata Gunas like Ruksha, Khara and Vishada.

5) Bala Samprapti : Bala Samprapti is a disease of chronic pattern

with few cardinal symptoms and Yapya Svabhava, hence

mostly require routine but regular treatment.

6) Kala Samprapti : In Sandhivata, Shula becomes worst towards

evening which indicates the predominance of Vata.

DISEASE PROCESS ACCORDING TO SHADKRIYAKALA

To have a clear understanding of the etiopathogenesis of

the disease Sandhivata and an attempt has been made to

understand the Samprapti of Sandhivata in the light of

Shadkriyakala.

1) Sanchaya (Stage of accumulation) : Indulgence in the

provocative factors result into the accumulation of the Doshas

which in turn affect the equilibrium. The affect can be

observed as a general vague body symptoms like Stabdha

Purna Kosthata, Pittavabhasata, Mandosmata etc. (Su. Su.

21/22). Whereas in a patient who ultimately becomes the

victim of Sandhivata, Vatavyadhi may be show the signs and

symptoms of Asthi Rukshata, Asthi Kharata and Asthi

Vishadata due to Vata Sanchaya in Asthi itself.

2) Prakopa (Stage of vitiation) : Failure to take a corrective

measures during the Sanchaya Avastha and allowed to act

further the Prakopa stage starts. In this stage already

accumulated Dosha get strengthened at their own seats and

tend to become excited. In this stage, due to provocation of

Vata, Kostha, Toda and Kostha Sancharana may be manifested

(Su. Su. 21/13). In a patient who is likely to develop

Sandhivata, we may see the Asthibheda Lakshana in this stage.

3) Prasara (Stage of spread) : In this stage, excited Dosha spreads

to other organs, structures and part of the body. If the

provocating factor are not checked followed by the failure of

physician to treat or to have a proper diagnosis (Su. Su.

21/14). Careful examination of patient who is going to disease

Sandhivata may disclose the Lakshanas like Pada-Prishtha-

Shirograha, Cheshta Alpata, spasticity and more severity of

previously existing signs and symptoms.

4) Sthana Sanshraya (Stage of localization) : As a continuation of

previous stages and conditions in this stage the spreading

Doshas become localized wherever, there is Kha-vaigunya or

reduced immunity, and it marks the beginning of specific

disease pertaining to that structure. This stage represents the

Purvarupa phase of disease and the interaction between the

Dosha and Dushya takes place (Su. Su. 21/15). If vitiated Vayu

localized in a joint they may cause Sandhivata. In this stage,

the Purvarupa of the disease occurs. We can see the Lakshana

of Sanga of Majjavaha Srotasa during this stage like Parvaruka Parvastambha, Parvabheda etc. (Ch. Su. 28/29; Su. Su. 15/9)

5) Vyakti (Stage of onset) :This stage may be stated as the

manifestation of the fully developed disease i.e. results of

Dosha Dushya Sammurchhana and it is represented by its

characteristic symptomatology i.e. Rupa. In case of

Sandhivata, patient feels Vedana like Prasarana and

Akunchana of Sandhi. On examination clinician can easily find

out Shotha which palpates likes air filled bag.

6) Bheda (Stage of complication) : This is the stage which needs

very careful handling. According to Sushruta, if the proper

management is not done at this stage the vitiated Doshas or

the disease may become incurable. At stage, the neglected

cases may get sever complications and metastatis etc. sublaxation,

deformity of the joints, loss of movement of the

joint, involvement of other joint and the chronicity of disease

can be understood at the stage of complication of the

Sandhivata.

SAMPRAPTI GHATAKA

Nidana (etiology) - Vata Prakopaka Nidana (Ch. Chi.28/15-18)

Dosha -Vata (particularly vyana vayu) and Kapha (Sleshaka)

Dushya -Asthi, Majja, Rasa and Meda

Srotasa -Asthivaha, Majjavaha, Rasavaha and Medovaha

Srotodushti -Sanga

Agni –Manda (mainly)

Doshamarga –Marmasthi Sandhi (according to Cha. Su. 17/112-113)

Rogamarga -Madhyama (Ch. Su. 11/48-49)

Udbhavasthana -Pakvashaya (Ch. Chi. 28/37)

Roga adhisthana -Asthisandhi

DIAGNOSIS OF SANDHIGATVATA

Sandhivata can be diagnosed by the use of various

Ayurvedic Pariksha and symptoms mentioned by classics.

Examination of Patients : No any specific Pariksha Vidhi for

Sandhivata is given in Ayurvedic texts. From the Lakshana given

by ancient and modern scientist, we can get clue for examination

of the sufferers, the main three types of examination are as

under.

1) Darshana Pariksha (Inspection) : In this examination,

physician should observe Shotha or Atopa (swelling) over

the affected joint, gait, attitude, muscular wasting etc.

2) Sparshana Pariksha (Palpation) : Acharya Charaka has

clearly mentioned the special symptom – Vatapurna Driti

Sparsha Shotha which can be palpable on joint, local

temperature with the back of palm, tenderness, crepitus

during passive movements, wasting of muscles, fixed flexion

of hip, lymph nodes.

3) Prashna Pariksha (History) : History of common symptoms

of like pain, onset, chronicity, joint involvement, stiffness,

mechanical disorders e.g. locking, giving way, click etc. and

lymph should be collected.

SAPEKSHA NIDANA (Differential Diagnosis)

The importance of Sapeksha Nidana lies in the establishing

the exact identity of the disease. Wherever, identical signs and

symptoms prevailing in two or more of the disease, the chances

of being misguided from arriving at a true diagnosis is indeed

great. Hence, differential diagnosis is invitiable for accurate

identity. Symptoms related to Sandhi are not only seen in

Sandhivata, but also in so many other conditions. Some of the

conditions in which Sandhi Pida and/or involvement of Sandhi

may present are as follow.

Sarvanga Kupita Vata (Ch. Chi. 28/24)

Kaphakshaya (A. S. Su. 19/5)

Mamsakshaya (A. S. Su. 19/6)

Medakshaya (Ch. Su. 17/65)

Asthikshaya (Ch. Su. 17/66)

Majjakshaya (Su. Su. 15/9)

Amavata (M. Ni. 25/7)

Vatarakta (Ch. Chi. 29/21)

Kostuka Shirsha (A. S. Ni. 15/54)

Sandhibhagna (B. P. II/48/2) etc.

A comparative study of cardinal feature of similar disease

entities are given below, for clear idea regarding the disease

Sandhivata under the caption of Sapeksha Nidana mainly

available and the nearest localized disorders of Sandhis are

presented as under.

SAPEKSHA NIDANA

Factors	Sandhigatavata	Amavata	Vatarakta	Kostukashirsha
Jwara	Absent	Present	Absent	Absent
Amapradhanya	Absent	Present	Absent	Absent
Hrid Gaurava	Absent	Present	Absent	Absent
Prone age	Old age mainly	Any age	Any age	Any age
Vedana	At prasarana & Akunchana pravriti	Sanchari & vrishchika danshavata	Mushika damshavata vedana	Tivra vedana
Shotha	Vatapurna Driti Sparsha	Sarvang and Sandhigata	Mandal yukta	Koshtruka Shirshvat
Sandhi	Weight bearing joints	Big Sandhi	Small Sandhi	Only Janu
Upashaya	Abyanga	Ruksha Svedana	Raktamokshan	Raktamokshan

SADHYASADHYATA

Sandhigata Vata is one of the Vatavyadhi described in all

Samhita and Sangraha Grantha. Acharya Vagbhatta and Sushruta

have considered Vata Vyadhi as Mahagada. It is so called due to

the fact that the treatment is time consuming and prognosis is

uncertain. Further, Dhatukshaya is the chief cause of Vata

Vyadhi. Dhatukshaya is difficult to treat as Acharya Vagbhatta

has elaborated that since body is accustomed to Mala.

Dhatukshaya is more troublesome than Dhatu Vriddhi.

Sandhigata Vata is one of the Vata Vyadhi, therefore it is Kashta

Sadhya.

The ailment of aged persons are Kashta Sadhya and

Sandhigata Vata is the affliction of elderly persons. Disease

situated in Marma and Madhyama Rogamarga is Kashta Sadhya.

Sandhigata Vata is the disease of Sandhi which forms Madhyama

Rogamarga. Further, Vatavyadhi occurring due to vitiation of

Asthi and Majja are most difficult to cure.

In the list of Kashta Sadhya Vata Vikara, Sandhigata Vata is

not mentioned by Acharya Charaka, but while commenting on

word ‘Khuda Vatata’ Chakrapani explains the meaning of Khuda

Vatata as Gulpha Vatata or Sandhigata Vatata. Thus, Sandhivata

can be considered as Kashta Sadhya Vata Vyadhi. It may be

curable if occurs in strong persons and if it is recently originated

and if there are no complications.

Osteoarthritis defferential diagnosis

Diagnostic considerations

The initial diagnostic goal is to differentiate osteoarthritis from other arthritides, such as rheumatoid arthritis. The history and physical examination findings are usually sufficient to diagnose osteoarthritis. Radiographic findings confirm the initial impression (see Workup), and laboratory values are typically within the reference range.

Rheumatoid arthritis

Rheumatoid arthritis predominantly affects the wrists, as well as the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints. It rarely, if ever, involves the distal interphalangeal (DIP) joints or the lumbosacral spine.

Rheumatoid arthritis is associated with prominent, prolonged (> 1 hour) morning stiffness and overtly swollen, warm joints. Radiographic findings include bone erosion (eg, periarticular osteopenia or marginal erosions of bone) rather than formation. Laboratory findings that further differentiate rheumatoid arthritis from osteoarthritis include the following:

·         Systemic inflammation (elevated erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP] level)

·         Positive serologies (rheumatoid factor [RF] or anti–cyclic citrullinated peptide [anti-CCP] antibodies)

·         Inflammatory joint fluid with a predominance of polymorphonuclear leukocytes (PMNs)

·         Elevated white blood cell (WBC) count

Additional arthritides

Back pain may result from spondyloarthropathy or from osteoarthritis with sacroiliac and lumbosacral spine involvement. Clinical history and characteristic radiographic findings can be used to differentiate these disorders.

Secondary osteoarthritis must be considered in individuals with any of the following:

·         Chondrocalcinosis

·         History of joint trauma

·         Metabolic bone disorders

·         Hypermobility syndromes

·         Neuropathic diseases

The following disorders should also be considered in the differential diagnosis:

·         Crystalline arthropathies (ie, gout and pseudogout)

·         Inflammatory arthritis (eg, rheumatoid arthritis)

·         Seronegative spondyloarthropathies (eg, psoriatic arthritis and reactive arthritis)

·         Septic arthritis or postinfectious arthropathy

·         Fibromyalgia

·         Tendonitis

In patients with knee pain, other disorders to consider in the differential diagnosis are patellofemoral syndrome & prepatellar bursitis.

Practice Essentials

 

Osteoarthritis is the most common type of joint disease, affecting more than 20 million individuals in the United States alone. It can be thought of as a degenerative disorder arising from the biochemical breakdown of articular (hyaline) cartilage in the synovial joints. However, the current view holds that osteoarthritis involves not only the articular cartilage but also the entire joint organ, including the subchondral bone and synovium.

Essential update: New AAOS guideline for knee osteoarthritis treatment

In June 2013, the American Academy of Orthopaedic Surgeons (AAOS) released a revised clinical practice guideline (CPG) on the treatment of osteoarthritis of the knee. The 2 key changes from their 2009 guideline are the following^[1] :

·         The recommended dosage of acetaminophen was reduced from 4,000 mg to 3,000 mg a day; this change is not specifically for osteoarthritis patients but reflects a change made by the FDA since 2009 for all individuals who use acetaminophen

·         Intra-articular hyaluronic acid is no longer recommended as a treatment for patients with symptomatic osteoarthritis of the knee

Other recommendations include the following:

·         Patients with only symptoms of osteoarthritis and no other problems, such as loose bodies or meniscus tears, should not be treated with arthroscopic lavage

·         Patients with a body mass index >25 should lose a minimum of 5% of their body weight

·         Patients should participate in low-impact aerobic exercise

·         Patients with symptomatic osteoarthritis of the knee can be treated with acetaminophen, intra-articular corticosteroids, or non-steroidal anti-inflammatory drugs (NSAIDs)

·         Custom-made lateral wedge insoles, glucosamine and/or chondroitin sulfate or hydrochloride, needle lavage, and acupuncture are not recommended

 

 

Signs and symptoms

Symptoms of osteoarthritis include the following:

·         Deep, achy joint pain exacerbated by extensive use - The disease’s primary symptom

·         Reduced range of motion and crepitus - Frequently present

·         Stiffness during rest (gelling) - May develop, with morning joint stiffness usually lasting for less than 30 minutes

Osteoarthritis of the hand

·         Distal interphalangeal (DIP) joints are most often affected

·         Proximal interphalangeal (PIP) joints and the joints at the base of the thumb are also typically involved

·         Heberden nodes, which represent palpable osteophytes in the DIP joints, are more characteristic in women than in men

·         Inflammatory changes are typically absent or at least not pronounced

Diagnosis

Osteoarthritis is typically diagnosed on the basis of clinical and radiographic evidence. No specific laboratory abnormalities are associated with osteoarthritis.

Imaging studies

·         Plain radiography - The imaging method of choice because radiographs are cost-effective and can be readily and quickly obtained; in the load-bearing areas, radiographs can depict joint-space loss, as well as subchondral bony sclerosis and cyst formation

·         Computed tomography (CT) scanning - Rarely used in the diagnosis of primary osteoarthritis; however, it may be used in the diagnosis of malalignment of the patellofemoral joint or of the foot and ankle joints

·         Magnetic resonance imaging (MRI) - Not necessary in most patients with osteoarthritis unless additional pathology amenable to surgical repair is suspected; unlike radiography, MRI can directly visualize articular cartilage and other joint tissues (eg, meniscus, tendon, muscle, or effusion)

·         Ultrasonography - No role in the routine clinical assessment of patients with osteoarthritis; however, it is being investigated as a tool for monitoring cartilage degeneration, and it can be used for guided injections of joints not easily accessed without imaging

·         Bone scanning - May be helpful in the early diagnosis of osteoarthritis of the hand; bone scans also can help differentiate osteoarthritis from osteomyelitis and bone metastases.

Arthrocentesis

The presence of noninflammatory joint fluid helps distinguish osteoarthritis from other causes of joint pain. Other synovial fluid findings that aid in the differentiation of osteoarthritis from other conditions are negative Gram stains and cultures, as well as the absence of crystals when fluid is viewed under a polarized microscope.

CHIKITSA

The aim of Chikitsa is to remove causative factor or disease

as well as restoration of the Doshika equilibrium. The elimination

of the disease can be achieved by Shodhana and Shamana.

Shodhana comprises of Antaha Parimarjana and Bahira

Parimarjana. Bahira Parimarjana is achieved by Snehana,

Swedana, Mardana, Lepana etc. Shamana types of Chikitsa cures

disease without eliminating Doshas.

In the management of Sandhivata, above three measures

are taken into consideration in the classics. Acharya Sushruta

was the first to explain the Chikitsa in detail. He preferred

Snehana, Upanaha, Agnikarma, Bandhana, Unmardana in case of

Vata located in Snayu Asthi and Sandhi.

Snehana : Snehana besides being the chief Purvakarma

procedure for the Panchakarma therapy, happens to be a one

of the most significant Chikitsa. Snehana therapy is

administered to persons in two different ways as follows.

1) External application (Abhyanga)

2) Internal application (Snehapana)

Both external and internal Snehana are effective in

Sandhivata.

Sneha Dravya possesses Drava, Sukshma, Sara, Snigdha,

Manda, Mrudu, Guru properties, which are due to predominance

of Jala and Prithvi Mahabhuta. Sneha alleviates Vata because

properties of Sneha are just opposite to those of Vata. The Vayu,

in its normal or undisturbed condition, maintains a state of

equilibrium between Dosha and Dhatu. Similarly it exercises

considerable influence on the functioning of Manasa. Hence, this

Vayu should be kept in stage of equilibrium for the individual to

be healthy and happy. Snehana helps in the promotion and

regulation of the proper functioning of Vayu.

It is stated that by the regular use of Abhyanga, all the

changes of old age could be prevented and cured, if are already

manifested. This Jarahara effect of Snehana is very important as

far as Sandhivata is concerned. It replenished the diminished

Dhatu, increases the Prana (vitality) and strength of Agni.

Upanaha : Upanaha is one of the four types of Sweda by

Acharya Sushruta, Swedana is the procedure which relieves

stiffness, heaviness, cold and induces sweating. It plays dual

role of Purvakarma and Pradhana Karma. Upanaha is

bandaging. Here a paste of the roots of the Vayu subduing

drugs is prepared and is then applied on the affected joints.

The paste should be hot and mixed with Sneha. After applying

the paste, the joint is covered with leaves and then it is

bandaged with cotton and leather. The duration of the bandage

is about 12 hours. The application of heat causes relaxation of

the muscles and tendon, improves the blood supply.

Agnikarma : Agnikarma on the affected joint relieves pain. To

perform Agnikarma on Sandhi, Kshudra, Guda and Sneha are

to be used. Acharya Kashyapa has contraindicated Agnikarma

on Shira Sandhi and Asthi. Here, Dalhana has elaborated the

fact that there is no need to perform Agnikarma on Shira Ashti

and Sandhi incase of disease affective them.

Bandhana : Bandhana is bandaging tightly leaves of

Vatashamaka drugs are bandaged tightly on affected Sandhi.

This bandaging does not leave any scope for Vata to inflate the

Sandhi. In Sandhigata Vata Shotha appears like a bag inflated

with air, Bandhana causes abatement in this Shotha.

Unmardana : This is the type of massage in which pressure is

exerted on diseased Sandhi. It relieves Shotha and enhances

blood circulation.

Basti : Since Sandhivata is disease of Madhyama Rogamarga,

Basti is the treatment of choice. In Sandhivata, Sneha Basti is

preferable considering the Dhatukshaya and old age of the

persons.

Yogasana may help for some extent in preventing and

curing of Sandhivata. The regular practice of Yogasanas

improves the symptoms in different ways like decreasing

overweight, decreasing laxity (Bhole – 1982). Posture will also

be improved by Yogasana (Yogendraji – 1984), which is also an

important predisposing factor in Sandhivata.

PATHYA-APATHYA

Specific Pathya and Apathya for Sandhivata are not

mentioned, but as this disease being a Vatavyadhi, we should

adopt same of general Vatavyadhi.

Pathya Ahara

Godhuma, Mamsa, Raktashali, Godugdha, Ajadugdha,

Ghrita, Draksha, Ama, Madhuka, Ushna Jala, Sura, Surasava,

Amlakanjika, Madhura – Amla – Lavana Rasa Pradhana Ahara are

Pathya.

Pathya Vihara

Atapa Sevana, Mrudu Shayya, Ushnodaka Snana etc.

Apathya Ahara

Yava, Kodrava, Chanaka, Kalaya, Sheeta Jala, Ati Madhya

Pana, Sushka Mamsa, Katu-Tikta-Kashaya Rasa Pradhana Ahara

are Apathya.

Apathya Vihara

Chinta, Ratri Jagarana, Vega Vidharana, Shrama, Anashana,

Vyavaya, Vyayama, Chankramana, Kathina Shayya are Apathya.

 From the modern standpoint, the disease osteoarthritis is

identical to Sandhi Vata is its signs and symptoms.

OA, a common degenerative disease of the joint, affects

approximately 10% of all the adults (man & women) and the

prevalence increases with the age. The disease is characterized by

focal areas of destruction of articular cartilage, sclerosis of the

bone and hypertrophy of the soft tissues. OA must commonly

affect the weight-bearing joints in particular the knee, hip and

spine and the interphalangeal joints of the hand. The wrist,

shoulder and ankle are less often involved. Not all the patients

with joint symptoms have radiographic changes and not all

radiographic changes are associated with symptoms.

THE STRUCTURE AND FUNCTION OF THE JOINT

Definition : An articulation (joint) is a point of contact between

bones, between cartilage and bones or between teeth and

bones. When we say that one bone articulates with another, we

mean that one bone forms a joint with another bone. The

scientific study of joint is called arthrology (Arthro = joint,

Logos = study of).

Synonyms : Articulation

Arthroses

Junction ossium

Classification of The Joints : The joints may be categorized

into structural, based on anatomical characteristic, or into

functional classes, based on the type of movement they

permit.

Structural Classification : The structural classification of joint

is based on the presence or absence of a space between the

articulating bones that is called synovial (joint) cavity and the

type of connective tissue that binds the bones together.

Structurally the joints are classified as –

a) Fibrous Joints : There is no synovial (joint) cavity and the

bones are held together by fibrous (colagenous) connected

tissue.

b) Cartilagenous Joints : There is no synovial cavity and the

bones are held together by cartilage.

c) Synovial Joints : There is a synovial cavity and the bones

forming the joints are united by a surrounding articular

capsule and frequently by accessory ligaments.

Functional Classification : The functional classification of joints

takes into account the degree of movement they permit.

Functionally a joint is classified as follows.

1) Synarthrosis : Syn = Together, Arthros = Joint

Synarthrosis is an immovable joint.

2) Amphiarthrosis : Amphi = On both sides, Arthros = Joint

An amphiarthrosis is a slightly movable joint.

3) Diarthrosis : Diarthros = Moveable joint

A diarthrosis is a freely movable joint.

ETYMOLOGY OF OSTEO-ARTHRITIS

The word osteoarthritis means –

a) Osteo – The word ‘osteo’ comes from the Greek word ‘Osteon’

means bone.

b) Arthritis – The prefix ‘Arth’ means joint. The suffix ‘itis’ is

defined as inflammation.

Hence, arthritis means inflammation of joint. So

osteoarthritis can be defined of as inflammation of the bony part

of the joints.

SYNONYMS OF OSTEO-ARTHRITIS

Osteoarthritis (First used by Garrode)

Arthritis deformans (Virchono 1852)

Degenerative arthritis

Hypertrophic degenerative chondro osteoarthritis (WEIL)

Arthrosis (Adams)

Hypertrophic arthritis (Bernard)

Degenerative joint disease (Baues and Barmett 1936)

Post traumatic arthritis (Adams)

There are many synonyms given by modern medical

workers for these degenerative disease.

DEFINITION OF OSTEO-ARTHRITIS

The scientific and medical definition of osteoarthritis is : -

It is one of the most common form of arthritis, which runs

chronic, slowly progressive course and usually affects almost all

the weight-bearing and frequently used larger joints of the

extremities with an exception to distal inter-phalangeal joints. It

is a degenerative joint disease, which affect the smaller joint of

the spine also. It is characterized clinically by pain, stiffness and

at times swelling of the joints. A pathologically it shows

degenerative changes in the articulating bones, together with

irregular hypertrophy of the bone and cartilages, giving rise to

osteophytes.

EPIDEMIOLOGY OF OSTEO-ARTHRITIS

OA is most common joint disease of human among the

elderly, knee OA is the leading cause of chronic disability in the

developed countries. Under the age of 55 years, the joint

distribution of OA in man and women is similar. In older

individuals hip OA is more common in man, while OA of

interphalangeal joints and the thumb based is more common in

women. Similarly radiographic evidence of knee OA and

especially symptomatic knee OA is more common in women than

in man.

In other cases, the relation of heredity to OA is less

ambiguous. Thus, the mother and sister of women with distal

interphalangeal joint OA (Heberden’s nodes) are respectively

twice and thrice as likely to exhibit OA in these joints as the

mother and sister of unaffected women.

Age is the most powerful risk factor of OA. In a radiographic

survey of women less than 45 years old, only 2% had OA, between

the age of 45 – 64 years. However, the prevalence was 30% and

for those older than 65 years it was 68%. In males, the figures

were similar, but somewhat lower in the older age groups.

Obesity is a risk factor for knee OA and hand OA. For those

in the highest quintal for body mass index (BMI) at base line

examination, the relative risk for developing knee OA in the

ensuing 36 years was 1.5 for man and 2.1 for women. Obesity

plays an even larger role in the etiology of the most serious case

of knee OA. Further, obese subjects who have not yet developed

OA can reduce their risk.

ETIOLOGY OF OSTEO-ARTHRITIS

Age : The process appear to begin in the second decade of life,

but degenerative changes are not apparent until middle age

and by 55 to 65 years of age approximately 85% have

roentgenologic evidence, to a variable degree of the disease.

Sex : Men and women are equally affected, up to 54 years of

age. The pattern of involvement is similar in both. Thereafter

the disease is more severe and more generalized in women.

Heredity : An epidemiologic study suggests that osteoarthritis

is an articular expression of a generalized constitutional

condition resulting from inherited metabolic abnormalities.

Heberden’s nodes may be inherited as a single autosomal gene,

sex influenced to be dominant in females and recessive in

males. The age at penetrance is variable. In elderly women

when penetrance is complete, the frequency due to the

dominant trait is 30% in man, as a result of the recessive trait,

the frequency is 3%. The exact mode of transmission is

unknown.

Obesity : The disease is twice as prevalent in the obese and

mainly affects the weight-bearing joints. In obese man, the

disease often assumes the generalized pattern move typical of

women.

Climate : In general, patients with degenerative disease are

less affected by changes in the whether than are patients with

Rheumatoid Arthritis. However, they frequently complaint of

more pain while in damp areas and cold.

Structure : The patient suffering from degenerative joint

disease are usually overweight hyperesthenic type, overall

muscular developmental with skeletal robustness, bigger,

heavier and more lateral in build their patients afflicted with

Rheumatoid Arthritis. Obesity poses as mechanical burden on

the joint undergoing abrasion.

Other Systemic Factor : In Women, a significant association

between hand disease and elevated serum cholesterol levels.

Hypertension has been associated with generalized

Osteoarthritis in man and knee Osteoarthritis in non-obese

women. Trauma is associated with development of

Osteoarthritis.

The Affect Of Arthritis On The Individual

Arthritis threatens the individuals’ physical, psychological,

social and economic well being (National Arthritis Plan, 1999).

Physical Impact : Pain, loss of joint motion, fatigue, resulting

in less physical activity than the rest of the adult population.

Inactivity puts arthritis sufferers at a higher risk for

premature death, heart disease, diabetes, high blood pressure,

colon cancer, obesity, depression and anxiety. Rheumatoid

arthritis patients are at further risk of shortened life spans

because of systemic complications of the disease and

complications of its treatment.

Pain is the major impact of arthritis. Factors that

contribute to pain include swelling of the joint, the amount of

heat or redness present, or damage that has occurred within

the joint. Each individual has a different threshold and

tolerance for pain, often affected by both physical and

emotional factors.

Psychological Impact : Stress, depression, anger, and anxiety

often accompany arthritis. Patients may have difficulty coping

with pain and disability, which can lead to feelings of

helplessness, lack of self-control and changes in self-esteem

and self-image.

Pain can be affected by the individual’s mental state,

including depression, anxiety, and even hypersensitivity at the

affected sites due to inflammation and tissue injury. The

increased sensitivity appears to affect the amount of pain

perceived by the individual (NIAMS, 2001).

Serious depression is extremely common among medically

ill geriatric patients. Geriatric patients have the highest rate

of completed suicide of any age group. Geriatric depression is

often overlooked by physicians or dismissed as an unavoidable

accompaniment to old age or medical illness. Physician visits

by patients who later complete suicide often center around

multiple somatic complaints and not around discussions or

evaluations of mood (McGann, p. 426). Physicians should be

aware of common classes of therapeutic drugs known to cause

depression in the elderly (including NSAIDS) (Mc Gann, p. 426).

Social impact: Social well-being is affected by arthritis. People

with arthritis frequently experience decreased community

involvement, difficulties in school, and sexual problems. These

social problems are often aggravated by a lack of

understanding and empathy among co-workers, employers,

teachers, school nurses and others.

Economic impact: Inadequate access to care, financial burdens

due to health care costs and income loss resulting from work

limitations. Arthritis is second only to heart disease as a major

cause of missed work.

CLASSIFICATION OF OSTEO-ARTHRITIS

1) Primary Osteoarthritis

a) Localized Osteoarthritis

b) Generalized Osteoarthritis (3 or more joint groups involved)

c) Erosive Osteoarthritis (Rare)

2) Secondary Osteoarthritis

a) Mechanical

i) Congenital and developmental disorders such as hip

dysplasias, slipped femoral epiphysis.

ii) Post traumatic

b) Post inflammatory and infective arthritis : Such as

Rheumatoid Arthritis, septic arthritis.

c) Neuropathic joint disease

d) Endochrine causes : Acromegaly, Cushing’s syndromes

e) Metabolic causes : Gout, Psudogout, Ochronosis

f) Iatrogenic causes, including intra-articular

CLINICAL SUBSETS

Localized OA : The joints are usually affected one at a time

over several years, with the distal interphalangeal joints (DIPs)

being more often involved than the proximal interphalangeal

joints (PIPs). The onset may be the painful and associated with

tenderness, swelling and inflammation and impairment of

hand function. The inflammation often occurs around the

female menopause. PIP – predominant nodal OA has a

superficial similarity to early Rheumatoid Arthritis. Even if a

weekly positive rheumatoid factor is found, it is of no

significance. The inflammatory phase settles after some

months or years, leaving painless bony swellings posterolaterly

– Hebendon nodes (DIPs) and Boucher’s nodes (PIPs), along

with stiffness and deformity. Functional impairment is slight

for most, although PIP – OA restricts gripping more than DIP

involvement. On x-ray, the nodes are marginal osteophytes

and there is joint space loss.

Carpometacarpal and metacarpophalangeal OA of the thumb

coexist with nodal OA and cause pain, which decreases as the

joint stiffens. The squared hand in OA is caused by bony

swelling of the carpometacarpal joint and fixed adduction of

the thumb. Function is rarely severely compromised.

Polyarticualr hand OA is associated with a slightly increased

frequency of OA at other sites.

HIP OA

Hip OA affects 7 to 25% of white adult Caucasians but it

significantly less common in black African population. There are

two major subgroups defined by the radiological appearance. The

most common is superior – pole hip OA, where joint space

narrowing and sclerosis predominantly affect the weight-bearing

upper surface of the femoral head and adjacent acetabulum. This

is most common in men and unilateral at presentation although

both hips may become involved because the disease is

progressive. Less commonly, medial cartilage loss occurs. This is

most common in women and associated with hand involvement

(nodal, generalized OA, NGOA) and is usually bilateral.

Knee OA

The prevalence of knee-OA is 40% in individuals aged over

75 years. It is commoner in women than men. There is a strong

relationship with obesity. The disease is generally bilateral and

strongly associated with polyarticular OA of the hand in elderly

women. The medial compartment is most commonly affected and

leads to a various (bow-legged) deformity. There is often also

retropatellar OA. Previous trauma, maniscal and cruciate

ligament tears and obesity are risk factor for developing knee OA.

Primary Generalized OA

This is less common than nodal OA of the hands but is

usually seen in combination. It is also called ‘nodal generalized

OA' (NGOA). It is predominantly affects women. The other joints

affected are the knees, first MTP and hip joints, and spondylosis.

There is a female preponderance and a strong familial tendency.

NGOA is associated with immune complex deposition and may

have an autoimmune cause. Its onset is often sudden and severe.

Erosive OA

There is rare. The DIPs and PIPs are inflamed and equally

affected. In contrast to nodal OA, the functional outcome is poor.

Radiologically, there are marked subchondral cysts. Erosive OA

may develop into RA and may not be a true subset of OA.

AETIO-PATHOLOGY

In modern medical science, to know the aetiopathology

clearly, some theories were put forward. They are –

Aging

Trauma

Physiologic stress and strain

Heredity

Metabolic disorders

Endochrine dysfunction

Focal infection

Vascular disorders

PATHOGENESIS

The main load on articular cartilage – the major target

tissue in Osteoarthritis – is produced by contraction of the

muscles that stabilize or move the joint. Although, cartilage is an

excellent shock absorber in terms of its bulk properties, at most

sites it is only 1–2mm thick – too thin to serve as the sole shock

– absorbing structure in the joint. Additional protective

mechanisms are provided by sub-chondral bone and peri-articular

muscles.

Articular cartilage serves two essential functions in the

joint, both of which are mechanical. First it provides a

remarkably smooth bearing surface, so that with joint movement

the bones glide effortlessly over each other with synovial fluid as

lubricant, the coefficient of friction for cartilage rubbed against

cartilage, even under physiologic loading is 15 times lower than

that of two ice cubes passed across each other. Second articular

cartilage prevents concentration of stresses, so the bones do not

shatter when the joint is loaded.

Osteoarthritis develops in either of two settings. 1) The bio

material properties of the articular cartilage and subchondral

bone are normal, but excessive loading of the joint causes the

tissue to fail or 2) The applied load is reasonable, but the material

property of the cartilage or bone are inferior.

Although articualr cartilage is highly resistance to wear

under conditions of repeated oscillation, repetitive impact

loading soon leads to joint failure. This fact accounts for the high

prevalence of Osteoarthritis at specific sites related to vocational

or avocational overloading. In general, the earliest changes occur

at the sites in the joints that are subject to the greatest

compressive load. More than 80% of all cases of idiopathic

Osteoarthritis of the hip may be due to subtle congenital or

developmental defects, such as congenital

subluxation/dislocation, acetabular dysplegia, legg-calve-perther

disease or slipped capital femoral epiphysis, which increase joint

congruity and concentrate the dynamic load.

Clinical condition that reduce the ability of the cartilage or

sub-chondral bone to deform are associated with development of

Osteoarthritis. In ochronosis, e.g. accumulation of homogentisic

acid polymers leads to stiffening of the cartilage. In osteopetrosis

stiffness of the sub-chondral trabeculae occurs. In both

conditions severe generalize apparent by the age of 40. If the subchondral

bone is stiffened experimentally, repetitive impact

loading soon leads to breakdown of the overlying cartilage.

Conversely osteo-porosis in which the bone is abnormally soft

may protects against Osteoarthritis.

PATHOLOGY

The most striking changes in Osteoarthritis are usually seen

in load-bearing area of the articular cartilage. In the easily stages,

the cartilage is thicker than normal but with progression of

Osteoarthritis, the joint surface thins, the cartilage softens, the

integrity of the surface is breeched and vertical clefts develop

(fibrillation). Deep cartilage ulcers, extending to bone, may

appear. Areas of fibro-cartilaginous repair may develop, but the

repaired tissue is inferior to pristine hyaline articular cartilage in

its ability to withstand mechanical stress. All of the cartilage is

metabolical active, and the chondrocytes replicate, forming

clusters (clones). Later, however, the cartilage becomes hypocellular.

Remodeling and hypertrophy of bone are also major feature

of Osteoarthritis. Appositional bone growth occurs in the subchondral

region, leading to the bony “sclerosis” seen

radiographically. The abrated bone under a cartilage ulcer may

take on the appearance of ivory (eburnation). Growth of cartilage

and bone at the joint margins leads to osteophytes, which alter

the controls of the joints and may restrict movement. Apathy

chronic synovitis and thickening of the joint capsule may further

restrict movement. Peri-articular muscle wasting is common and

may play a chief role in symptoms and as indicated above in

disability.

INVOLVEMENT OF SPECIFIC JOINTS

Knee : The knee is most commonly affected joint. One or both

knees may be involved. Patients experience difficulty in

ascending or descending stairs or standing up from the

squatting posture. There may be isolated involvement of the

medial compartment of the tibio-femoral or patello-femoral

joint, or both. Progressive disease leads to the deformities and

joint instability. There may be inability to extend and flex the

knee fully. X-ray examination shows narrowing of the joints

space and calcification in the cruciate ligaments and the

patellar ligaments. The changes are often marked in the

patello-femoral area.

Hip : In India, Osteoarthritis of the hip is less common than

that of the knee. True hip pain is felt on the outer aspect of

the growing or inner thigh. Occasionally, the pain of hip joint

disease may be referred to the lumbo-sacral area or to the

knees. There is limitation of joint movement. The patient

walks with a characteristic antalgic gait. Rontgen examination

of degenerative hip joint shows narrowed or absent joint space,

sclerosis of bone and marginal exostoses. The decrease in joint

space is seen especially in the weight bearing portion of the

femoral head and acetabulum.

Hand : Usually the distal interphalangeal and first

carpometacarpal joints are involved. Heberden node over the

region of the distal interphalangeal and bouchered nodes over

the proximal interphalangeal joints may be seen. Often the

pain is maximum at the beginning. Deformities may be

developed.

Spine : Spondylosis is the term applied to degenerative

changes affecting the disc and vertebral bodies. The main

symptoms of degenerative spinal joints are localized or

radicular pain, stiffness, limitation of motion and muscular

spasm. The osteophytes thus formed may cause mechanical

compression of vital structures such as the spinal cord, nerve

involving apophysial joints may take place in the cervical,

thoresic and lumber spines. Patients may be asymptomatic

even in the presence of radiological changes in the spine.

When patients are symptomatic, the pain may be localized to

vertebral or paravertebral areas. The patient may present with

radicular nerve involvement or spinal cord compression.

Foot : The metatarso phalangeal joint of one or both big toes is

affected after an injury or recurrent attack of gout and

produce hallur rigidus.

CLINICAL FEATURES

1) Pain : Pain is a cardinal symptom of degenerative joint disease

which occurs on use (friction effect) and is relieved by rest.

Later as the disease progresses, pain occurs even at rest. The

severity various from a slight dull ache to a severe sharp pain.

2) Swelling : Swelling may occur, when the joint is enlarged.

Swelling usually feels hard. Distention of a joint is due to a

thickened synovial membrane and to the occurrence and acute

effusion. Joints may show localized tenderness.

3) Stiffness : Stiffness is felt after resting or when first getting

out of bed.

4) Crepitus : Crepitus may be felt or even heard. It can be

detected by feeling the joint with one hand while it is moved

passively with the other.

5) Restricted Movements : Movement in the affected joints

increasingly limited, initially as a result of the pain and

muscular spasm, but later because of capsular fibrosis,

osteophyte formation and remodeling of bone.

6) Deformity : Considerable deformity may result from the

weakness of the muscles and ligaments and from the

absorption of the ends of bones, so that displacement and even

shortening occurs.

HEBERDEN’S NODES

This is a commonest manifestation of Osteoarthritis. This is

a cartilaginous and bony enlargement of the terminal

interphalangeal joint of the fingers. It is characterized by

presence of small, hard nodular swelling in the vicinity of

affected joints. Particularly on their dorsolateral surface. Similar

nodes on the proximal interphalangeal joints are often called

“Bouchard’s nodes”.

Heberden’s nodes may be single, particularly following

trauma, but usually are multiple. Generally they affect several of

the fingers but are more commonly found in the index and middle

fingers. Women are affected much more than men. They are

usually painless, but may be painful and produce numbness and

tingling in the fingers.

 True or Primary Heberden’s Nodes – when Heberden’s node

appear spontaneously i.e. without a history of previous injury.

 Traumatic Heberden’s Nodes – Nodes appear after the injury.

E.g. baseball injury or the catching of a finger in a door etc.

LABORATORY FINDINGS

The diagnosis of Osteoarthritis is usually based on clinically

and radiographic features. In the early stages, the radiograph may

be normal, but joint space narrowing becomes evident as articular

cartilage is lost. Other characteristic radiographic finding include

subchondral bone sclerosis, subchondral cyst and osteophytosis.

Although, tibio-femoral joint space narrowing has been

considered to be a radiographic surrogate for articular cartilage

thinning, in patient with early Osteoarthritis who do not have

radiographic evidence of bony changes (e.g. subchondral sclerosis

or cysts or osteophytes), joints spaces narrowing alone does not

accurately indicate the status of the articular cartilages.

Similarly, osteophytosis alone in the absence of other

radiographic features of Osteoarthritis. More than 90% of persons

over the age of 40 years have some radiographic changes of

Osteoarthritis in weight bearing joints only 30% of these persons

are symptomatic.

No laboratory studies are diagnostic for Osteoarthritis, but

specific laboratory testing may help in identifying one of the

underlying causes of secondary Osteoarthritis because, primary

Osteoarthritis is not systematic. The erythrocytes sedimentation

rate (E.S.R.), serum chemistry determination, blood counts and

urine analysis are normal. Analysis of synovial fluid reveals mild

leucocytosis, with a predominance of mononuclear cells. Synovial

fluid analysis is of particular value in excluding other conditions

such as calcium pyrophosphate dehydrate (C.P.P.D.) deposition

disease, gout or septic arthritis. S. calcium, uria, proteins,

albumin-globumin ratio, S. phosphatase and G.T.T. are fall within

normal limits (Karsley – 1937). S. cholesterol and blood sugar

may be slightly elevated, indicates its degenerative origin.

o MRI can demonstrate early cartilage changes.

o Arthroscopic can reveal early fissuring and surface erosion

of the cartilage.

ROENTGENOGRAPHIC FINDINGS

Early, the x-ray appearance is normal. Then joint narrowing

gradually appears, reflecting thinning of the articular cartilage

covering opposing subchondral corties. Finally, with advanced

progression of the disease, the joint interval is markedly

narrowed, articular margins are sharp, osseous spores or

osteophyte appear at the margins, the subchondral bones become

wide and sclerotic and bones cysts appear in the subchondral

bone at areas of maximum pressure. A negative film does not rule

out the disease. On the other hand a film with typical

characteristic of Osteoarthritis does not necessarily define this as

the primary disease. Degenerative are frequently superimposed

on the disease, notably gout, infectious arthritis and Rheumatoid

Arthritis.