Pain and lameness in a joint can have many etiologies:

Infection of the synovial space/joint capsule can initiate migration 
of macrophages to the site to phagocytize the pathogen.  Macrophage 
activity will result in increased pus/debris in the joint.  As a 
consequence of this, inflammation and hypoxia can develop.  
Cartilage can be destroyed by oxygen-derived free radicals produced 
by the phagocytes as well as by enzymes produced by the 
chondrocytes.  This can result in a decreased blood supply as 
vessels grow deeper into bone and limit nutrients reaching 
cartilage.  Lack of nutrients to the cartilage can cause local 
erosion of the cartilage layer.

Pressure stress can be caused by the above sequence of events or by 
outside trauma causing stress on the joint.  Increased pressure on 
the joint can result in compression, which leads to further hypoxia 
and damage.  Early subchondral bone sclerosis can decrease the shock 
absorption capacity of the joint resulting in tensile failure of the 
matrix collagen.  Decreased matrix proteoglycan and collagen can 
lead to increased water absorption ultimately resulting in swelling 
and softening of the bone and tissue.

Cartilage destruction by mechanical forces is probably via insults 
to subchondral bone, synovium, or chondrocytes.

The above etiologies can cause pain by leading to localized 
swelling, pressure increase in the joint with movement, and 
decreased shock absorption of the cartilage.

Pain caused by the above factors can result in lameness as movement 
will exacerbate inflammation and pressure at the joint.  In 
response, the animal will reducing the amount of weight carried on 
the affected limb.

Malformation of joints.

There are two possible etiologies of joint malformation.

Intrinsic, which would be due to genetic factors.

Extrinsic, which would be due to external factors.

Joint malformation in which the bones do not articulate properly can 
cause stress and pressure as mentioned above and cause pain.