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Australian immigrants may be at lower risk of melanoma compared to individuals born in Australia. Melanoma incidence rates increase with age in both sexes, with a sharper rise in incidence rates observed in males over 60. Melanoma is now the third most common malignancy in Australia for both sexes, behind colorectal, breast and prostate cancer. Latitude of residence correlates well with UV exposure even though it does not account for individual behaviours or migration from areas of different UV indices. For the purposes of this risk model, Australia has been divided into 3 zones based on latitudes of the eastern states.
Naevus counts are primarily genetically determined, though UV exposure plays a role in initiating naevus development and growth. Naevus count on the arms (from elbow to shoulder, not forearm) correlates well with total number of naevi and is simpler to assess that total body count. The presence of clinically atypical naevi is more strongly correlated with risk for melanoma than common naevi4. It is important to note that, whilst atypical naevi are a significant risk factor, the majority of melanomas (43 - 77%) arise de novo and dysplastic naevi do not warrant prophylactic excision. Melanoma risk increases with freckle density, usually assessed on the shoulders and upper back. Hair colour was selected for this risk model as an easily assessed phenotypic characteristic. From the few studies available, it is difficult to assess the extent to which past history acts as an independent risk factor. DescriptionMetatarsal fractures are common injuries to the foot often sustained with direct blows to the foot or twisting forces.A If adequately assessed these fractures are easy to treat and have a favorable prognosis. The overall increase in incidence of melanoma is almost entirely attributable to rising incidence in people over 60 years. In Australia, 1 in 14 males and 1 in 22 females will develop invasive melanoma in their lifetime (to age 85). Red hair has also been shown to be the phenotypic trait best representing the presence of MC1R variants, a known genetic marker of melanoma risk5. Risk for a further melanoma increases progressively with increasing numbers of primary melanomas.
Incidence of second primaries also peaks around the ages of 25-34, which may reflect the association with cases of familial melanoma.

There is evidence that it is a strong risk factor and we felt it was important to include it in this model.
It is difficult to tease out the proportion of risk that can be attributed to susceptibility genes versus pigmentary characteristics (also genetically determined) and environmental factors.
Individuals with known mutations that predispose to melanoma make up a small proportion (around 2%) of individuals with a positive family history. Mutations in CDKN2A may be found in 25 to 40% of members of melanoma-prone families, with CDK4 mutations much less common. They must be distinguished from solar lentigines which persist indefinitely and result from a severe sunburn or chronic solar damage. Those diagnosed with their first melanoma before age 45 have about twice the risk of a second primary as the older group. Despite this, studies consistently show that melanoma in a first degree relative (parent, sibling, child) increases risk of melanoma approximately 2 fold6.
Freckle density is greater with proximity to the equator, hence there is a correlation with latitude6. It has been reported that 10.5% people with multiple melanoma have a positive family history. While this impacts on absolute risk prediction it has little or no bearing on the model's ability to discriminate between individuals of high and low risk. The likelihood of finding a mutation in CDKN2A rises from about 5% in families with 2 affected members, to 20-40% if 3 or more family members are affected9. Two sesamoid bones under the head of the 1st metatarsal bear approximately one third of the body weight. UV radiation causes DNA damage and mutations in tumor suppressor and proto-oncogenes responsible for unrestricted cell turnover. Furthermore, residence in areas with high rates of melanoma significantly increases the penetrance (ie. The anterior tibialis attaches to the inferomedial base, functioning in elevation of the 1st metatarsal and supination of the forefoot.
Peroneous longus attaches on the proximal lateral base, functioning in plantar flexion of the first metatarsal and pronation of the forefoot. There are no interconnecting ligaments between the 1st and 2nd metatarsals, allowing for independent motion. Injuries to the 1st metatarsal are usually due to direct trauma and are often open or comminuted.

The dorsalis pedis artery and deep peroneal nerve are in this area, and branches of the superficial peroneal nerve are around the deeper structures and must be protected during surgery.The 5th metatarsal has tendinous attachments consisting of the peroneal brevis tendon, which inserts over the dorsolateral tuberosity, and the peroneus tertius tendon, which attaches on the dorsal aspect of the metaphysis and the lateral band of the plantar aponeurosis.
A strong band of the plantar aponeurosis connects the projecting part of the tuberosity with the lateral process of the tuberosity of the calcaneus.A Dorsal, plantar, and interosseus ligaments attach between the base of the fourth and fifth metatarsals. Articulations in the area consist of the articulations between the bases of the fourth and fifth metatarsals and the fifth metatatarsal and cuboid bone. Fractures of the 5th metatarsal account for approximately 25% of all injuries to the metatarsals. Blood is primarily supplied from a single artery that enters at the junction of the proximal and middle thirds of the diaphysis and supplies the shaft.
Zone 2 is at the metaphyseal-diaphyseal junction, distal to the cancellous (styloid) tuberosity, and zone 3 is on the diaphysis, distal to the peroneus tertius.
Fractures involving Zone 2, called Jones fractures, are particularly susceptible to nonunion and malunion because this diaphyseal bone is a watershed region between two blood supplies and because like zone 3 it is often subject to significant repetitive forces. Most metatarsal shaft fractures are caused by direct or indirect trauma to the foot.A Direct impact causes a transverse or comminuted fracture pattern, while an indirect twisting-type injury causes an oblique or spiral fracture pattern with soft-tissue swelling. If the patient is able to evert the foot, the injury will likely heal with non-operative treatment. Weakness in eversion is often noted as the pull of the peroneus brevis tendon displaces fracture fragments.A Figure 2.
Radiograph of Dancera€™s fracture - Zone 1 of 5th metatarsalTrue Jones fractures occur in Zone 2 of the fifth metatarsal and the fracture line extends through the proximal articulation with the fourth metatarsal. If possible the radiographs should be performed with weight-bearing to help assess displacement and instability. Except in the case of an isolated direct blow to the foot, initial films should include the entire foot to rule out associated injuries that may require treatment. Weight-bearing x-rays can be particularly helpful when trying to rule out of assess Lisfranc injuries.Figure 3. In rare instances severely comminuted fractures which are unable to be fixed with lag screws may be treated with external fixation.
If there are no signs of instability and no associated injuries to the midfoot or other metatarsals, these fractures can be managed with a short leg cast or removable boot with weight bearing as tolerated for 4-6 weeks.

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