FOOT & ANKLE PAIN
Foot and ankle pain can have a big impact on your mobility and quality of life, making it difficult to stay active or even get through a normal day. From plantar fasciitis and Achilles tendinopathy to ankle sprains and flat feet, our osteopaths and remedial massage therapists at Dingley Health Hub are experienced in treating a wide range of foot and ankle complaints. We'll assess not just the site of your pain but how the rest of your body may be contributing, and provide hands-on treatment and practical guidance to help you recover fully and move with ease again.
Common Foot & AnkleConditions
Ankle sprain
Lateral ankle sprains are among the most common musculoskeletal injuries worldwide, affecting people of all ages and activity levels — from elite athletes to people who simply step off a kerb awkwardly. They involve stretching or tearing of the lateral ankle ligaments, most commonly the anterior talofibular ligament (ATFL) and the calcaneofibular ligament (CFL), through sudden inversion and plantarflexion of the foot. Ankle sprains are graded I (ligament stretching with intact structural integrity), II (partial ligament tearing with mild instability) and III (complete ligament rupture with significant instability). Despite being frequently labelled a minor injury, inadequately rehabilitated ankle sprains result in chronic ankle instability in up to 40% of cases — making thorough rehabilitation essential, not optional.
Symptoms include:
Immediate lateral ankle pain at the moment of injury, rapid swelling over the lateral malleolus, bruising that can track down into the foot and up the lower leg within 24–48 hours, tenderness on palpation of the ATFL and CFL, and pain with weight-bearing ranging from mild discomfort (Grade I) to complete inability to bear weight (Grade III). A positive anterior drawer test — the talus slides forward relative to the tibia — indicates significant ATFL disruption and is used to assess the degree of instability. Bony point tenderness over the malleoli or base of the fifth metatarsal should prompt X-ray to exclude fracture (Ottawa Rules).
How we treat it:
Optimal loading — progressively exposing the injured ankle to controlled stress — is the current evidence-based approach and produces superior outcomes to complete rest or immobilisation alone. In the first 48–72 hours, protection from re-injury, gentle range of motion exercises within a comfortable range, compression bandaging and elevation manage the acute inflammatory response. Early talocrural and subtalar joint mobilisation, beginning within the first week, accelerates restoration of ankle dorsiflexion and reduces the residual joint stiffness that is one of the main causes of chronic ankle instability. Peroneal muscle strengthening — the dynamic evertor muscles that protect the lateral ankle — combined with progressive single-leg balance and proprioception training restores the neuromuscular control that is the ankle's primary defence against future sprains. Grade II–III sprains receive a structured 6–8 week rehabilitation program that progressively advances from balance on a stable surface to balance on unstable surfaces, lateral agility drills and sport-specific cutting movements before return to play. Ankle taping and bracing guidance is provided for the return-to-sport transition period.
Chronic ankle instability
Chronic ankle instability (CAI) develops when one or more ankle sprains fail to fully rehabilitate, leaving the lateral ankle ligaments with inadequate tensile strength and — critically — the neuromuscular control of the ankle significantly impaired. The peroneal muscles lose both their reaction speed and their strength following ankle sprain, and without specific rehabilitation this deficit persists indefinitely, leaving the ankle vulnerable to re-injury from even minor provocations. Many people simply accept that their ankle "gives way" regularly and treat subsequent sprains as an inevitable inconvenience — but targeted rehabilitation can substantially reduce recurrence risk and, in most cases, restore full functional stability without surgery.
Symptoms include:
A persistent subjective sense of instability — the ankle giving way or feeling unreliable — particularly on uneven surfaces, during direction changes and when descending stairs. Recurrent ankle sprains occurring with progressively less force (stepping off kerbs, walking on grass) compared to the original injury. Reduced confidence in the ankle during sport, hiking and everyday activities. Aching or discomfort after prolonged standing or walking. In some cases, residual swelling and stiffness around the lateral ankle from the accumulated effects of multiple sprains.
How we treat it:
The rehabilitation program for chronic ankle instability targets both the structural deficit (ligament laxity) and the neuromuscular deficit (impaired peroneal reaction speed and strength) that together create the instability. Progressive peroneal and tibialis posterior strengthening — beginning with seated resistance exercises and advancing to standing and single-leg functional movements — rebuilds the dynamic stabilisers that compensate for the lax ligament. A systematically progressed proprioception program — advancing from double-leg balance on a firm surface, to single-leg balance with eyes closed, to balance on an unstable surface (wobble board, foam), to dynamic balance tasks — restores the somatosensory function of the lateral ankle structures. Manual therapy addressing residual posterior talar and subtalar joint stiffness corrects the altered joint mechanics that impair proprioceptive input. Ankle bracing or taping during high-risk activities (sport, hiking) provides supplementary support during the rehabilitation period. Surgical lateral ankle stabilisation (Broström-Gould repair) is reserved for cases with confirmed structural ligament laxity that have failed a minimum of 3–6 months of comprehensive conservative rehabilitation.
High ankle sprain (syndesmotic injury)
A high ankle sprain — or syndesmotic injury — involves damage to the ligaments binding the distal tibia and fibula together: the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL) and the interosseous membrane. The mechanism is external rotation of the foot relative to the lower leg, most commonly occurring in contact sports (AFL, rugby, soccer), skiing and snowboarding. High ankle sprains are significantly more serious than lateral ankle sprains, requiring substantially longer rehabilitation (6–12 weeks compared to 2–4 weeks for lateral sprains) and carrying a much higher risk of long-term complications including syndesmotic widening, chronic pain and early ankle OA if not properly diagnosed and managed. They are frequently under-diagnosed in the acute setting, being mistaken for lateral ankle sprains or simply labelled a "bad sprain."
Symptoms include:
Pain localised above and anterior to the lateral malleolus — higher up the ankle than a typical lateral ankle sprain — rather than directly over the lateral malleolus itself. Significant pain with external rotation and dorsiflexion of the foot. A positive squeeze test (compressing the fibula against the tibia at mid-calf reproduces distal ankle pain) and a positive external rotation stress test. A characteristic clinical sign: the athlete is able to walk with minimal pain but cannot sprint, cut or push off at full speed — indicating the syndesmosis is disrupted under high load but stable under low load.
How we treat it:
Accurate diagnosis is the essential first step. We perform specific syndesmotic clinical tests and arrange weight-bearing X-ray to assess for diastasis — a widening of the distal tibiofibular joint that indicates complete syndesmotic disruption. Diastasis requires urgent surgical stabilisation with a syndesmotic screw or tightrope device; without surgery, the ankle joint will remain permanently unstable and painful. For stable high ankle sprains without diastasis, management follows a structured rehabilitation protocol: a controlled weight-bearing progression protecting the healing syndesmosis in the early weeks, progressive ankle stabilisation exercises and lower limb strengthening as healing progresses, and a functionally guided return to running and sport based on symptom resolution and performance on hop testing and change-of-direction tasks — not time alone. We communicate with the surgeon throughout where operative management is required.
Ankle osteoarthritis
Ankle osteoarthritis is far less common than hip and knee OA and is predominantly post-traumatic in aetiology — the long-term consequence of previous ankle fractures, severe ligamentous instability and recurrent sprains, or osteochondral lesions of the talus. Unlike hip and knee OA, which are primarily degenerative, approximately 70–80% of ankle OA cases have a clear traumatic history. Despite its different aetiology, ankle OA causes significant functional limitation because the ankle bears enormous forces during gait — up to 5–6 times body weight — meaning even moderate cartilage loss produces pain with daily walking. Anterior impingement from tibiotalar osteophytes causing restricted dorsiflexion is a characteristic and often overlooked feature.
Symptoms include:
Anterior ankle pain and stiffness — particularly a loss of ankle dorsiflexion that makes walking uphill, climbing stairs and squatting difficult or painful. An antalgic gait with reduced push-off from the affected ankle. Pain and stiffness that is typically worse after prolonged rest and improves briefly with gentle movement before worsening again with continued activity. Visible joint swelling after walking. Audible or palpable crepitus with ankle movement. In advanced cases, visible joint enlargement and deformity. Anterior impingement — a sharp pain and blocked sensation at the front of the ankle at end-range dorsiflexion — in cases with significant osteophyte formation.
How we treat it:
Anterior-posterior talar joint mobilisation is highly effective for ankle OA — restoring the posterior glide of the talus that is lost with arthritic joint changes and directly improving dorsiflexion range. This technique consistently provides meaningful pain relief and functional improvement. Gastrocnemius and soleus flexibility work addresses the equinus contracture — abnormal plantarflexion tightness — that is a consistent finding in ankle OA and that dramatically increases anterior impingement forces. Calf and peroneal strengthening maintains the muscular support needed for functional ambulation. A heel raise in the shoe reduces the range of dorsiflexion demanded at the ankle during normal gait, providing a simple and cost-effective symptom management strategy. Activity pacing advice — identifying which activities are tolerable and which provoke significant flare-ups — helps patients remain active without repeatedly loading the arthritic joint beyond its tolerance. Total ankle replacement (arthroplasty) and tibiotalar fusion both produce good outcomes for end-stage ankle OA, and we provide pre-surgical optimisation and comprehensive post-surgical rehabilitation for both procedures.
Ankle fracture rehabilitation
Ankle fractures — involving the medial malleolus, lateral malleolus or both (bimalleolar), and in some cases the posterior malleolus (trimalleolar) — are among the most common fractures presenting to emergency departments. Unstable fractures require surgical fixation with plates and screws (ORIF — open reduction and internal fixation). Following a period of cast immobilisation, the ankle is almost universally stiff, weak and swollen, with an altered gait pattern that does not resolve spontaneously without targeted rehabilitation. The consequences of under-rehabilitating an ankle fracture — persistent stiffness, weakness, altered mechanics and accelerated post-traumatic OA development — are significant and largely preventable with prompt, structured rehabilitation.
Post-immobilisation rehabilitation goals include:
Restoring full ankle dorsiflexion, plantarflexion, inversion and eversion; normalising the talocrural and subtalar joint mechanics that are disrupted by both the fracture and the immobilisation; rebuilding calf, peroneal and tibialis anterior strength; normalising the heel-toe gait pattern and push-off mechanics that are invariably altered after ankle fracture; recovering single-leg balance and proprioception to reduce long-term re-injury risk; and managing the persistent oedema that commonly remains for weeks to months after immobilisation.
How we treat it:
Joint mobilisation of the talocrural and subtalar joints — begun as early as weight-bearing allows — restores the restricted range of motion efficiently and prevents the progressive capsular fibrosis that develops with prolonged immobilisation. Progressive calf strengthening, advancing from seated calf raises to standing bilateral raises to single-leg standing calf raises, systematically rebuilds the plantarflexion strength critical for normal gait and stair negotiation. Gait retraining addresses the antalgic heel-toe pattern and reduced push-off that persist after fracture and, if left uncorrected, contribute to altered loading of the knee and hip. Progressive single-leg balance and proprioception training reduces the long-term re-injury risk that follows ankle fracture. For patients who have undergone surgical fixation, scar tissue management around the incision prevents adhesion of the scar to the underlying structures. We align all progression decisions with the surgeon's weight-bearing instructions and communicate proactively when we identify concerns.
Peroneal tendon injuries
The peroneus longus and peroneus brevis tendons run together in a fibro-osseous groove posterior to the lateral malleolus — held in place by the superior peroneal retinaculum — before diverging to their separate insertions on the foot. They are the primary dynamic stabilisers of the lateral ankle, acting as powerful evertors that resist the inversion forces most likely to cause ankle sprains. Peroneal tendon pathology takes three main forms: tendinopathy from repetitive overload (common in runners with varus foot posture and in people who perform excessive lateral training), acute tears from an inversion ankle sprain, and subluxation (dislocation of the tendons out of their groove behind the lateral malleolus). Peroneal pathology is significantly under-diagnosed — persistent lateral ankle pain, swelling or weakness following an apparently healed ankle sprain should always raise suspicion of peroneal tendon involvement.
Symptoms include:
Pain and tenderness along the course of the peroneal tendons — posterior and inferior to the lateral malleolus — rather than directly over it (which would suggest lateral ligament sprain). Swelling along the tendon course. Weakness and pain with resisted foot eversion. A snapping, clunking or popping sensation behind the lateral malleolus with ankle movement — the hallmark of peroneal tendon subluxation, where the tendons flick out of their groove. Worsening of symptoms with activities requiring powerful ankle eversion and inversion control, such as running on cambered surfaces and lateral sport movements.
How we treat it:
Peroneal tendinopathy is managed with a progressive loading program for the evertors — beginning with isometric peroneal contractions in the least provocative position and advancing through isotonic exercises to eccentric loading and functional sport-specific tasks. Shockwave therapy is incorporated for chronic peroneal tendinopathy where degeneration has reduced the tissue's capacity for spontaneous repair. Lateral heel wedging — raising the lateral aspect of the foot — reduces the compressive load on the peroneal tendons in their groove and provides meaningful symptom relief during rehabilitation. Footwear assessment addresses footwear-related contributors, particularly excessively worn lateral heel counters that create varus position loading the tendons. Peroneal tendon subluxation that is recurrent and symptomatic typically requires surgical repair of the superior peroneal retinaculum — a day procedure after which we provide comprehensive post-surgical rehabilitation. Ultrasound imaging is coordinated when there is diagnostic uncertainty, as it provides excellent real-time assessment of tendon integrity, thickness and dynamic subluxation.
Achilles tendinopathy
Achilles tendinopathy is one of the most common lower limb overuse injuries, with a lifetime incidence of approximately 24% in recreational runners and significantly higher rates in elite-level running and jumping athletes. It presents in two clinically distinct patterns that require different management approaches. Mid-portion Achilles tendinopathy — the most common form — affects the tendon body 2–6 cm above the calcaneal insertion and responds well to eccentric and heavy slow resistance loading. Insertional Achilles tendinopathy affects the tendon at its attachment to the calcaneus and is driven by a combination of tensile loading and compressive loading from the heel counter of the shoe and the dorsiflexion end-range position — making the eccentric loading approach used for mid-portion tendinopathy actively provocative and counterproductive for insertional cases. Correctly differentiating the two patterns at assessment is essential for applying the right treatment.
Symptoms include:
Morning stiffness in the Achilles tendon — often described as a stiff, creaky feeling in the back of the heel after the first few steps out of bed — that characteristically eases after 5–10 minutes of walking. A "warm-up effect" during exercise where pain improves after the first 10–15 minutes of activity before returning after exercise stops. Visible or palpable tendon thickening — a localised swelling in the tendon body (mid-portion) or at the heel bone attachment (insertional). Tenderness on palpation at the specific location. Pain that progressively worsens with increasing training load. A positive Royal London Hospital Test (squeezing the thickened mid-portion of the tendon at 90 degrees of dorsiflexion reduces the pain) helps confirm mid-portion tendinopathy.
How we treat it:
For mid-portion Achilles tendinopathy: the Alfredson eccentric heel drop protocol — lowering the heel below the step on a single leg, 3 sets of 15 repetitions twice daily over 12 weeks — is the gold-standard evidence-based rehabilitation exercise and produces durable tendon remodelling. Heavy slow resistance (HSR) training — including bilateral and then unilateral calf raises with progressive load — is an equally effective and more comfortable alternative. For insertional Achilles tendinopathy: flat-surface loading only (no step), isometric calf holds and progressive HSR are used, carefully avoiding the dorsiflexed position that compresses the tendon insertion. A heel raise (5–10 mm) in both shoes reduces the compressive load on the insertion. Shockwave therapy is incorporated for both patterns in chronic or recalcitrant cases — particularly for insertional tendinopathy where the response to loading alone is often slower. Footwear assessment ensures heel counters are not excessively compressing the insertion. We monitor rehabilitation progress and guide return to running using the VISA-A questionnaire — a validated tendinopathy severity score — and a structured walk-run program.
Plantar fasciitis
Plantar fasciitis is the most common cause of heel pain, affecting approximately 10% of the population at some point in their lifetime and accounting for around 1 million GP visits per year in Australia. Despite its name implying inflammation, the contemporary understanding of the condition is that it involves degenerative fasciopathy — structural breakdown and failed healing of the plantar fascia at its calcaneal origin — rather than a primary inflammatory process. The correct clinical term is therefore plantar fasciopathy. The plantar fascia is a thick band of fibrous connective tissue that runs from the medial calcaneal tubercle to the base of the toes, providing essential tension to the medial arch of the foot during the push-off phase of gait. Risk factors include obesity (each kilogram of additional body weight significantly increases plantar fascia loading), prolonged standing on hard surfaces, sudden large increases in walking or running activity, pes planus (flat foot), pes cavus (high-arched foot) and gastrocnemius tightness that reduces ankle dorsiflexion.
Symptoms include:
Sharp, stabbing heel pain with the very first steps after getting out of bed in the morning or after any prolonged period of rest — the hallmark symptom of plantar fasciitis and what most patients describe as their worst pain of the day. The pain typically eases after a few minutes of walking as the fascia warms and loosens, but returns and worsens again after prolonged standing, walking or at the end of an active day. Point tenderness that is precisely localised to the medial calcaneal tubercle — the bony attachment of the plantar fascia on the front-inner aspect of the heel — distinguishing plantar fasciitis from fat pad syndrome (where tenderness is central under the heel). Pain that worsens significantly with barefoot walking on hard floors, first thing in the morning.
How we treat it:
High-load plantar fascia strengthening — performed as a single-leg heel raise with a towel rolled under the toes to tension the plantar fascia — is the most evidence-supported rehabilitation exercise for plantar fasciopathy and produces significantly better long-term outcomes than stretching, orthoses or rest alone. Calf strengthening exercises address the consistent finding of gastrocnemius and soleus tightness that reduces ankle dorsiflexion and increases plantar fascia load during gait. A plantar fascia-specific night splint holds the foot in dorsiflexion overnight, maintaining the fascia at a lengthened position during sleep and dramatically reducing the severity of the first-step morning pain that patients find most debilitating. Shockwave therapy — applied directly to the calcaneal insertion of the plantar fascia — is highly effective and produces durable, long-term pain relief and fascial healing. It is supported by multiple level 1 randomised controlled trials and is our treatment of choice for plantar fasciopathy that has persisted beyond 3 months. Prefabricated or custom foot orthoses provide short-term symptom reduction by redistributing plantar pressure away from the painful insertion, used as an adjunct while the fascia is being rehabilitated. Low-dye calcaneal taping provides immediate mechanical unloading and pain relief. We achieve excellent outcomes without corticosteroid injection or surgical plantar fascia release in the vast majority of cases.
Heel fat pad syndrome
The heel fat pad is a highly specialised and complex shock-absorbing structure comprising fibro-elastic septa that enclose fat globules within discrete compartments, collectively capable of absorbing the enormous compressive forces generated at heel strike during walking and running. With advancing age, repetitive high-impact loading, prolonged standing on hard surfaces and certain systemic conditions such as rheumatoid arthritis, the heel fat pad progressively atrophies — losing volume, elasticity and its shock-absorbing capacity. This leaves the calcaneal periosteum and subchondral bone relatively unprotected from impact forces. Heel fat pad syndrome is significantly more common in older adults (particularly those over 60), distance runners logging high weekly mileage and people who stand for long hours on concrete or other hard surfaces. It is frequently misdiagnosed as plantar fasciitis — the distinction is clinically important as the management differs substantially.
Symptoms include:
A deep, bruised, aching or burning pain directly under the centre of the heel that is present throughout standing and walking — not just with the first steps after rest as in plantar fasciitis. The pain is often described as "walking on a stone" or as though the protective padding has been worn away, because functionally it has been. Tenderness on direct pressure over the central heel pad, distinct from the medial calcaneal tubercle tenderness of plantar fasciitis. Pain that worsens progressively with longer periods of standing and walking, and that is notably worse on hard floors and in thin-soled shoes.
How we treat it:
Unlike most other musculoskeletal conditions where progressive loading is the cornerstone, heel fat pad syndrome requires a protection and offloading approach — the atrophied pad cannot be regenerated with exercise. Silicone heel cups are the primary treatment: they redistribute the plantar pressure across a wider area of the heel, reducing the peak pressure on the atrophied central fat pad and providing immediate and meaningful pain relief in the majority of patients. A comprehensive footwear assessment is essential — thin-soled, unsupportive footwear dramatically worsens fat pad syndrome and switching to shoes with adequate heel cushioning can alone produce substantial improvement. Activity modification reduces cumulative impact loading during the rehabilitation period, with guidance on safe walking distances and surfaces. Running biomechanics are assessed and corrected where an excessive rear-foot strike pattern is amplifying heel impact forces. Insoles with central heel cutouts — removing all pressure from the most painful area of the heel — can be effective for severe cases.
Heel spurs
Calcaneal heel spurs are bony outgrowths (enthesophytes) that develop at the calcaneal enthesis — the bone-tendon or bone-fascia junction — in response to chronic tensile stress on the attaching soft tissue. They occur in two distinct locations: inferior heel spurs develop at the origin of the plantar fascia on the medial calcaneal tubercle and are found in association with plantar fasciitis; posterior heel spurs develop at the Achilles tendon insertion and are found in association with insertional Achilles tendinopathy. Both types are far more common than most people realise — they are present in approximately 15–25% of the general adult population on plain X-ray, and the vast majority of people who have them are entirely asymptomatic. When they do cause pain, it is almost always the surrounding inflamed or degenerated soft tissue driving the symptoms — not the bony spur itself.
Symptoms include:
Heel pain in the distribution of the associated soft tissue pathology — either plantar heel pain at the medial calcaneal tubercle (inferior spur and plantar fasciitis) or posterior heel pain at the Achilles insertion (posterior spur and insertional tendinopathy). Importantly, pain is not proportional to spur size — radiologically large spurs are frequently completely painless, while small spurs associated with actively inflamed soft tissue can be very painful. Most patients first become aware of their heel spur incidentally, when an X-ray ordered for heel pain reveals its presence.
How we treat it:
The heel spur itself does not require treatment in the vast majority of cases — it is the associated plantar fasciopathy or insertional Achilles tendinopathy that generates the pain, and treating this soft tissue pathology reliably resolves the pain regardless of the spur's presence. Shockwave therapy applied to the heel produces excellent and durable results for both inferior and posterior symptomatic heel spurs — it treats the degenerative soft tissue pathology at the enthesis and is supported by strong clinical evidence. Heel cushioning and footwear modification provide meaningful symptom relief during treatment. Patient education is one of the most valuable interventions we provide in this context: clearly explaining that the spur does not need surgical removal, that the pain is coming from the soft tissue and not the bone, and that conservative treatment produces excellent outcomes in the vast majority of cases — significantly reduces the anxiety and unnecessary treatment-seeking that heel spur diagnoses frequently generate.
Sever's disease (calcaneal apophysitis)
Sever's disease — the most common cause of heel pain in children and adolescents aged 8–14 — is a traction apophysitis of the calcaneal growth plate (apophysis) at the posterior heel, where the Achilles tendon attaches. During periods of rapid skeletal growth, the calcaneal apophysis is significantly weaker than the surrounding mature bone, the Achilles tendon and calf muscles — creating a structural mismatch where the powerful traction forces generated during running and jumping repeatedly stress and irritate the vulnerable growth plate. Sever's disease is more common in boys than girls (reflecting their later skeletal maturity and longer window of apophyseal vulnerability), and is associated with high levels of physical activity in running and jumping sports. It affects both heels in approximately 60% of cases. It is a completely self-limiting condition that resolves fully with skeletal maturity when the apophysis fuses to the underlying calcaneus — typically between ages 14–16 in girls and 16–18 in boys.
Symptoms include:
Posterior heel pain at the back and bottom of the heel — over the calcaneal apophysis — that develops during and after physical activity, particularly running, jumping and kicking. Pain that may cause a limp during or after sport in more severe cases. A strongly positive calcaneal squeeze test — compressing the sides of the posterior heel between the examiner's fingers firmly reproduces the pain and is the most reliable diagnostic clinical finding. Pain with standing on tiptoe (heel raises). Symptoms that are typically worse during and immediately after activity and ease with rest, and that often flare significantly during growth spurts when the Achilles tendon-to-bone length discrepancy is at its greatest.
How we treat it:
Sever's disease is managed with intelligent, activity-preserving load management — not complete rest, which is both unnecessary and counterproductive to the child's physical and social wellbeing. The first step is identifying a tolerable activity level that keeps symptoms manageable while maintaining meaningful sport participation, and building from there. During acute flares, we reduce the volume and intensity of jumping and high-speed running — the most provocative activities — while maintaining lower-intensity training, games participation and non-impact activities such as swimming and cycling where possible. Gastrocnemius and soleus stretching is addressed systematically, as calf muscle tightness — which dramatically increases during growth spurts as the bone grows faster than the muscle-tendon unit — directly amplifies the traction force on the apophysis. Progressive calf and lower limb strengthening builds the muscle's ability to absorb and attenuate the forces transmitted to the apophyseal attachment. A simple 5–10 mm heel raise — either in both shoes or as an insole insert — temporarily reduces the Achilles traction force on the apophysis and provides quick and meaningful pain relief. A patellar (infrapatellar) strap worn around the lower leg can provide additional symptom control during sport participation. Ice applied to the posterior heel for 10–15 minutes after activity reduces post-exercise soreness. Thorough, age-appropriate education for both the child and their family about the self-limiting nature of the condition, its expected timeline and the safety of continued sport participation is one of our most valued contributions — it significantly reduces the anxiety that this diagnosis often generates.
Shin Splints
Medial tibial stress syndrome (MTSS) — universally known as shin splints — is a diffuse periosteal stress reaction along the posteromedial border of the tibia, caused by repetitive tibial bending forces that exceed the bone's capacity for adaptive repair and remodelling. It is the most common running injury in new runners and military recruits beginning a running program, accounting for up to 35% of running injuries in these populations. MTSS is not simply "muscle soreness" — it represents genuine bone stress, and it exists on a continuum that, if the loading stimulus is not appropriately reduced, can progress to a frank tibial stress fracture. Accurate differentiation between MTSS and tibial stress fracture is therefore clinically important and influences management significantly.
Symptoms include:
A diffuse, aching or burning pain along the inner border of the lower leg — typically extending over a broad area of 5 cm or more along the posteromedial tibia — that is present during running and eases with rest. Tenderness to palpation along this same broad segment of the posteromedial tibial border, which is a key clinical differentiator from tibial stress fracture (where tenderness is localised to a single focal point). The absence of pain at rest in the early stages, with pain only during and after running. Symptoms that are typically worst at the start of a run, improve during the middle of the run, and return after stopping. Progressive worsening if training loads are not modified. Focal point tenderness, night pain or pain at rest should always prompt urgent MRI to exclude stress fracture.
How we treat it:
An immediate reduction in running load is the essential first intervention — continuing to run through MTSS without load modification reliably results in progression to stress fracture. We design a structured walk-run program that progressively re-exposes the tibia to impact loading at a rate that allows bone adaptation, rather than the abrupt load increases that caused the injury. Hip abductor and calf strengthening corrects the biomechanical deficits — excessive knee valgus, rearfoot overpronation and weak hip abductors — that increase the tibial bending moment during running and are consistently identified in runners with MTSS. Running gait assessment addresses crossover gait (where the feet land across the midline, increasing tibial torsion forces) and overstriding (where the foot lands too far in front of the body, increasing impact loading). Bone stress nutrition is systematically reviewed — calcium and vitamin D intake, total energy availability and any features of relative energy deficiency in sport (RED-S) that may be reducing the bone's capacity for adaptive repair. When symptoms are atypical, progress is slower than expected, or focal tenderness is identified, we coordinate MRI or bone scan with the patient's GP to exclude stress fracture before returning to running. Most runners with MTSS achieve a full return to their pre-injury training volume within 4–8 weeks with this approach.
Frequently asked Questions
Can osteopathy help with foot and ankle pain?
Answer:
Yes. Osteopathy is highly effective for the full range of foot and ankle conditions. Our osteopaths assess not just the painful site but the entire lower limb — including ankle and foot joint mobility, calf and intrinsic foot muscle strength, footwear, gait mechanics and how the knee, hip and spine may be contributing to the load passing through your foot and ankle. Treatment includes joint mobilisation to restore ankle and foot movement, soft tissue therapy and dry needling to release tight calf and foot muscles, progressive strengthening and proprioception programs, and shockwave therapy for chronic tendon and fascia conditions such as plantar fasciitis and Achilles tendinopathy. Whether you have a recent ankle sprain, chronic heel pain, a running injury or a growth-related condition in a child, we create a treatment plan tailored to your specific diagnosis and activity goals.
I rolled my ankle — how do I know if it's serious or just a sprain?
Answer:
Most ankle injuries are lateral ankle sprains involving the ligaments on the outer ankle, and the majority can be safely managed without imaging. However, certain signs should prompt an X-ray to exclude fracture — known clinically as the Ottawa Ankle Rules. These include bony tenderness directly over the tip of either ankle bone (the malleoli), bony tenderness at the base of the fifth metatarsal (the outer midfoot bone), or an inability to bear weight for four steps both immediately after the injury and at assessment. Significant swelling, bruising tracking into the foot, and pain with the anterior drawer test (the foot sliding forward relative to the shin) indicate a more significant ligament injury — Grade II or III — that requires structured rehabilitation. If you are unsure, a same-day clinical assessment will determine whether imaging is needed and get appropriate treatment started immediately, which is important — early treatment significantly reduces the 40% risk of developing chronic ankle instability after an inadequately rehabilitated sprain.
Why does my ankle keep giving way even though it healed months ago?
Answer:
This is the hallmark of chronic ankle instability, and it is extremely common after an ankle sprain that wasn't fully rehabilitated. When a sprain occurs, the peroneal muscles on the outer ankle lose both their strength and — critically — their reaction speed. If this neuromuscular deficit isn't specifically addressed with proprioception training, it persists indefinitely, regardless of how long ago the original injury occurred or how settled the pain feels. The ankle ligaments may also retain some residual laxity. The combination leaves the ankle vulnerable to giving way on uneven surfaces, during direction changes or descending stairs — often from forces far smaller than the original injury. The good news is that targeted rehabilitation — progressive peroneal strengthening combined with a systematically progressed balance and proprioception program — restores functional stability in the majority of cases without surgery, even years after the original sprain.
What is the difference between plantar fasciitis and heel fat pad syndrome?
Answer:
These two conditions are frequently confused but have a key distinguishing feature: the timing and location of pain. Plantar fasciitis causes sharp, stabbing pain with the very first steps in the morning or after rest — the hallmark "first-step pain" — that eases after a few minutes of walking, with tenderness localised to the medial calcaneal tubercle (the front-inner part of the heel). Heel fat pad syndrome causes a deep, bruised or aching pain directly under the centre of the heel that is present throughout standing and walking, not just with first steps, often described as "walking on a stone." The treatment approaches differ significantly: plantar fasciitis responds to high-load fascia strengthening, night splinting and shockwave therapy, whereas fat pad syndrome — where the natural cushioning has atrophied and cannot be regenerated with exercise — is managed with heel cushioning, silicone heel cups and footwear modification. Correct diagnosis is essential because treating one condition as the other will not produce results.
How long does plantar fasciitis take to go away?
Answer:
With appropriate treatment, most people see meaningful improvement within 6–8 weeks, though plantar fasciopathy that has been present for several months can take 3–6 months for full resolution — the longer it has been present, the longer it generally takes to settle. The most effective treatment combines high-load plantar fascia strengthening (a single-leg heel raise with a towel rolled under the toes), calf strengthening, a night splint to address the morning first-step pain, and shockwave therapy — which is supported by multiple high-quality clinical trials and is our treatment of choice for cases that have persisted beyond three months. Foot orthoses and taping provide useful short-term symptom relief while the underlying fascia is being rehabilitated, but they are an adjunct rather than a complete solution on their own. Consistency with the loading program is the single biggest factor in how quickly plantar fasciitis resolves.
What is the warm-up effect with Achilles tendon pain, and what does it mean?
Answer:
The "warm-up effect" is a characteristic pattern of Achilles tendinopathy where pain is present at the start of exercise, decreases or disappears once the tendon has warmed up during the first 10–15 minutes of activity, and then returns — often more intensely — after exercise stops, with stiffness particularly noticeable the next morning. This pattern is a useful diagnostic clue and distinguishes tendinopathy from acute injuries, where pain typically worsens with continued activity rather than improving. Importantly, the warm-up effect can be misleading — feeling better during exercise does not mean the tendon is fine, and continuing high training loads because "it warmed up" is a common reason tendinopathy becomes chronic. The correct response to the warm-up effect is to use it as a signal to begin progressive tendon loading — either the Alfredson eccentric heel drop protocol for mid-portion tendinopathy or flat-surface isometric loading for insertional tendinopathy — rather than as permission to continue training at the same intensity.
My child has heel pain after sport — could it be Sever's disease?
Answer:
Quite possibly. Sever's disease is the most common cause of heel pain in children and adolescents aged 8–14, and the pattern is very characteristic: pain at the back and bottom of the heel that develops during and after running, jumping and kicking, often affecting both heels. The squeeze test — gently compressing the sides of the heel between the fingers — reliably reproduces the pain and is the key diagnostic finding. It occurs because the growth plate at the heel (the calcaneal apophysis) is temporarily weaker than the surrounding bone and the Achilles tendon during growth spurts, creating a traction injury with running and jumping. It is more common in boys, completely self-limiting, and resolves fully once the growth plate fuses — typically by the mid-to-late teenage years. The most important point for parents is that complete rest is not necessary: with appropriate activity load management, calf stretching and a heel raise, most children can continue playing sport throughout their recovery while symptoms settle.
What's the difference between shin splints and a stress fracture?
Answer:
This distinction is clinically important because the management is very different. Shin splints (medial tibial stress syndrome) cause a diffuse aching or burning pain along a broad area — typically 5 cm or more — of the inner shin bone, with tenderness spread across that same broad area on palpation. The pain is present during running and eases with rest, and is typically worst at the start of a run, improves during the run, and returns afterwards. A tibial stress fracture, by contrast, causes pain that is localised to a single focal point on the bone, with tenderness concentrated at that specific spot rather than spread over a wide area. Crucially, stress fracture pain tends to be present at rest and may be present at night — something shin splints typically are not. Shin splints exist on a continuum that, if running load is not reduced, can progress to a stress fracture — so any focal point tenderness, night pain or pain at rest should prompt an urgent MRI to exclude stress fracture before continuing to run.
Should I get a heel spur removed surgically?
Answer:
In almost all cases, no — and this is one of the most important things we explain to patients who discover they have a heel spur, often incidentally on an X-ray taken for heel pain. Heel spurs are present in 15–25% of the general adult population, and the large majority of people with them have absolutely no pain. When a heel spur is associated with pain, it is almost always the surrounding soft tissue — the plantar fascia (inferior spurs) or Achilles tendon (posterior spurs) — that is generating the symptoms, not the bony spur itself. Importantly, pain is not proportional to spur size: large spurs are frequently painless, while small spurs with actively inflamed soft tissue can be very painful. Treating the underlying plantar fasciopathy or Achilles tendinopathy with shockwave therapy, progressive loading and footwear modification reliably resolves the pain regardless of whether the spur is still present on a follow-up X-ray. Surgical removal carries real risks and recovery time, and is essentially never the first — or even the tenth — line of treatment.
Do I need a referral to see an osteopath for foot or ankle pain?
Answer:
No referral is needed. You can book directly online at dingleyhealthhub.au1.cliniko.com/bookings or by calling (03) 9551 7110. Same-week appointments are usually available. Osteopathy and remedial massage for foot and ankle conditions are covered by most Australian private health insurance funds with appropriate extras cover — we have HICAPS on-site for on-the-spot claiming. WorkCover and TAC patients are welcome and managed with full documentation. If imaging such as X-ray, ultrasound or MRI is required to confirm a diagnosis — for example to exclude a fracture or characterise a tendon injury — we will advise you and coordinate this through your GP.