Stage 4 hallux rigidus may be treated via fusion of the joint (arthrodesis) or implant arthroplasty in which both sides of the joint are resurfaced or a hinged implant is used. Fusion of the joint is often viewed as more definitive but may lead to significant alteration of gait causing postural symptomatology. The implants termed "two part unconstrained" implants in which a "ball" type device is placed on the first metatarsal head and "socket" portion on the base of the big toe do not have a good long term track record. The hinged implants have been in existence since the 1970s, have been continually improved and have the best record of improving long term function. Another example of MTP joint implant is "Roto-glide" which is designed to restore optimum anatomical movement whilst preserving as much primary bone stock as possible.Cartilage replacement may be the first step before considering Fusion ( Arthrodesis- stiff toe joint) or arthroplasty. Cartilage repair for focal osteochondral defects of the first MTP may be a strategy before fusion or arthroplasty. Osteochondral plugs and resurfacing both have advocates. Although still at the case report stage, the experience is improving in the literature. References
External links

Hallux rigidus and cheilectomy at the Duke University Health Systems Orthopedics program
Overview at aaos.org
When as described; the condition is due to a saturation in the neural portion of the retina and not due to the absence of the photoreceptors per se.In general, the molecular pathomechanism of achromatopsia is either the inability to properly control or respond to altered levels of cGMP; particularly important in visual perception as its level controls the opening of cyclic nucleotide-gated ion channels (CNGs). Decreasing the concentration of cGMP results in closure of CNGs and resulting hyperpolarization and cessation of glutamate release. Native retinal CNGs are composed of 2 α- and 2 β-subunits, which are CNGA3 and CNGB3, respectively, in cone cells. When expressed alone, CNGB3 cannot produce functional channels, whereas this is not the case for CNGA3. Coassembly of CNGA3 and CNGB3 produces channels with altered membrane expression, ion permeability (Na+ vs. K+ and Ca2+), relative efficacy of cAMP/cGMP activation, decreased outward rectification, current flickering, and sensitivity to block by L-cis-diltiazem.Mutations tend to result in the loss of CNGB3 function or gain of function—often increased affinity for cGMP—of CNGA3. cGMP levels are controlled by the activity of the cone cell transducin, GNAT2. Mutations in GNAT2 tend to result in a truncated and, presumably, non-functional protein, thereby preventing alteration of cGMP levels by photons. There is a positive correlation between the severity of mutations in these proteins and the completeness of the achromatopsia phenotype.Molecular diagnosis can be established by identification of biallelic variants in the causative genes.