Indian pet parents examining their Labrador puppy's joints at home -- guide to congenital bone disorders in dogs before buying a puppy.

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Congenital Bone and Joint Disorders in Dogs: What to Know Before Buying a Puppy

Jun 07 • 10 min read

You have found the breed you want. The breeder is friendly, the puppy photos are adorable, and you are ready to say yes. But before you do, there are questions worth asking , not to scare you, but to protect you and your dog from a future that involves surgeries, lifelong pain management, and a bill you were not prepared for.

Congenital and inherited bone and joint disorders affect a significant number of dogs in India. Many are breed-specific, entirely predictable, and often visible in the puppy's family history , if you know what to look for. This guide explains each major condition, which breeds are at highest risk, and what responsible ownership and breeding actually look like.

Key Takeaways

Congenital means present at birth; inherited means passed through genes. Many skeletal disorders in dogs are both.
The most commonly encountered conditions in Indian dogs are hip dysplasia, osteochondrosis (OCD), patellar luxation, and elbow dysplasia , all with strong genetic components.
According to the Merck Veterinary Manual, congenital defects in dogs are estimated to occur in 0.2% to 3.5% of all canine births.
Genetic health screening of the breeding parents is the single most effective tool to reduce the risk of inheriting these conditions.
Most of these disorders cannot be reversed once established. The goal is always early detection, early management, and informed buying decisions.
Excess calcium supplementation in large breed puppies can worsen the severity of conditions like hip dysplasia and OCD , a common, preventable mistake in Indian homes.

What Does "Congenital" vs "Inherited" Actually Mean?

These two words are often used together but mean different things.

A congenital disorder is one that is present at birth. It developed during the puppy's time in the womb. Congenital does not automatically mean genetic. A mother that contracts a viral infection during pregnancy, or eats certain toxic plants, can produce puppies with malformed musculoskeletal systems, according to the Merck Veterinary Manual. These cases are not inherited; they are environmental.

An inherited disorder is one caused by genes passed from parent to offspring. The puppy is born with the genetic blueprint for a condition, even if that condition does not become visible for months or years. Hip dysplasia is a perfect example: the puppy looks normal at 8 weeks, but the genetic predisposition is already set.

Many of the disorders in this blog are both: congenital (present at birth or appearing very early) and inherited (with a clear genetic basis). That combination is what makes breed selection and health-screened breeding so important.

How These Disorders Show Up in Puppies

Not every congenital skeletal disorder is obvious from day one. Some reveal themselves gradually as the puppy grows and begins to bear weight and move.

Early signs that something may be wrong:

Limping or holding up a leg before 6 months of age
Uneven muscle development: one limb visibly thinner than the other
Difficulty rising from a lying position, or a "waddling" hind-end gait
Reluctance to climb stairs, jump, or run despite otherwise good health
Pain or crying when touched around the joints, spine, or limbs
Bowing or twisting of the limbs in a young puppy
Unusually frequent fractures with minimal trauma

Any of these signs in a puppy under 12 months warrants a veterinary visit. Many conditions are significantly better managed when caught at 4 to 8 months rather than at 2 years.

Hip Dysplasia: India's Most Common Inherited Joint Problem

Hip dysplasia is almost certainly the most talked-about congenital joint condition in India and with good reason. It is extremely common, affects many of the most popular breeds in Indian cities, and causes lifelong pain if not managed correctly.

According to the Merck Veterinary Manual, hip dysplasia is a common developmental disorder in which the femur (the upper leg bone) does not fit properly into the hip socket. This eventually leads to arthritis. An increased risk of the disorder can be inherited in many large breeds.

The hip joint is a ball-and-socket. In a healthy dog, the ball fits smoothly inside the socket. In a dog with hip dysplasia, there is looseness at that joint. The ball partially slides out. As the dog moves, the joint surfaces grind against each other. Over months and years, the cartilage wears away and the bone itself changes shape.

The Merck Veterinary Manual's veterinary edition explains that hip dysplasia results from the combined effect of many genes that influence skeletal development, connective tissue, and biomechanics. This polygenic inheritance involving many genes, not just one explains why even carefully bred dogs can develop the condition and why it has been so difficult to eliminate from popular breeds entirely.

What influences severity: Genetics sets the foundation, but several environmental factors determine how severe the condition becomes. Excessive and rapid growth, over-nutrition, and the wrong type of exercise during the growth phase can all worsen outcomes in a genetically predisposed puppy. Dogs carrying the gene that are kept at an ideal body weight and given controlled, low-impact exercise consistently fare better than their overweight counterparts.

Which breeds in India are most at risk: German Shepherd Dogs, Labrador Retrievers, Golden Retrievers, Rottweilers, and Great Danes carry the highest prevalence of hip dysplasia. The highest prevalence overall is seen in breeds that are stocky, round, and heavy-built, according to Merck. These are also among the most purchased breeds in Indian cities, which is why this condition is so commonly seen in Indian veterinary clinics.

Signs to watch for:

A "bunny-hopping" gait: the dog moves both hind legs forward together rather than alternating
Stiffness after rest, especially first thing in the morning
Reluctance to climb stairs, run, or jump
Visible muscle loss over the hips and hindquarters
Pain on hip manipulation

Screening: Responsible breeders use X-ray scoring systems (OFA in the USA, BVA in the UK) to assess breeding stock before mating. In India, veterinary orthopaedic X-rays of both parents before breeding can provide meaningful information. A puppy from two parents with good hip scores has a significantly lower risk than one from unscreened parents.

Management: Mild to moderate cases are managed with weight control, controlled exercise, physiotherapy, joint supplements like glucosamine-chondroitin, and anti-inflammatory medication when needed. Severe cases in young dogs may be candidates for surgical intervention. Once osteoarthritis has developed, management becomes lifelong.

Diagram comparing healthy dog hip joint versus hip dysplasia showing femoral head displacement.

Elbow Dysplasia: The Forelimb Version Nobody Talks About Enough

While hip dysplasia gets most of the attention, elbow dysplasia is equally common in large-breed dogs and arguably more disabling early in life, because the elbow is a forelimb joint that bears significant weight during every step.

According to the Merck Veterinary Manual, elbow dysplasia is a developmental orthopedic condition in which multiple abnormal processes can occur in the elbow joint. These include:

Medial coronoid disease (MCD): Fragmentation or erosion of a small bony process inside the elbow joint. The Merck Manual identifies this as one of the most common manifestations of elbow dysplasia in dogs.
Osteochondrosis of the elbow: Abnormal cartilage development at the medial part of the humeral condyle, leading to cartilage flaps or loose joint fragments.
Ununited anconeal process (UAP): A bony fragment inside the elbow that fails to fuse during development.
Elbow joint incongruity: A mismatch in the shape of the radius and ulna bones, creating uneven joint loading.

These conditions are most frequently seen in young, rapidly growing, large and giant-breed dogs, typically between 5 and 10 months of age. The Merck Manual specifically identifies Labrador Retrievers, Golden Retrievers, Bernese Mountain Dogs, and Rottweilers as high-risk breeds. Published research shows elbow dysplasia prevalence of up to 70% in Bernese Mountain Dogs and 17-30% in Labradors in screened populations.

Signs to watch for in a young dog:

Forelimb lameness, often worse after exercise
Stiffness after rest
Elbow held outward from the body
Pain when the elbow is flexed or extended
Swelling around the elbow joint

Diagnosis and treatment: CT scanning is now the preferred diagnostic tool for elbow dysplasia, offering much more detailed information than X-rays alone. Treatment depends on which component of elbow dysplasia is present but typically involves arthroscopic surgery to remove cartilage fragments and smooth damaged joint surfaces, combined with long-term joint support and physiotherapy.

Osteochondrosis (OCD): When Cartilage Fails to Become Bone

Osteochondrosis, or OCD (Osteochondritis Dissecans) when the cartilage detaches, is a developmental disorder where the immature joint cartilage fails to convert properly into bone during rapid growth.

The Merck Veterinary Manual describes it clearly: osteochondrosis is most commonly seen in large and giant breeds. The condition affects bone formation in the early stages of life, roughly 4 to 8 months of age, when a dog is growing at its fastest and the stress to the immature skeleton is greatest. The immature joint cartilage may separate from the underlying bone. This detached cartilage floats loosely in the joint cavity, where it causes inflammation, debris, and further interference with normal bone formation.

It most often affects the shoulder, elbow, knee, and tarsal (ankle) joints, in decreasing order of frequency, according to Merck.

Think of it like this. During normal growth, the soft cartilage at the joint surface gradually converts to hard bone. In OCD, some of that cartilage stays soft and then cracks under the weight of an active, fast-growing puppy. A piece breaks off and floats inside the joint. That loose fragment, sometimes called a "joint mouse," causes pain every time the joint moves.

Contributing factors beyond genetics: Rapid growth, over-feeding (especially excess calcium and energy during growth), and trauma. This is not purely a genetic condition: even a genetically normal dog can develop OCD if over-supplemented during the growth phase.

Signs:

Lameness in a young dog, typically 4 to 8 months
Pain on manipulation of the shoulder or elbow
Swelling and heat in the affected joint
Exercise intolerance

Treatment: Surgical removal of the cartilage flap or loose fragments via arthroscopy. Conservative management can work in very mild cases but carries the risk of ongoing joint inflammation.

Patellar Luxation: The Skipping Knee of Small Dogs

Small dog holding up hind leg showing classic patellar luxation posture in Indian Spitz breed.

Patellar luxation means the kneecap (patella) pops out of its groove. It is one of the most common orthopaedic conditions diagnosed in dogs, particularly in small and toy breeds.

The Merck Veterinary Manual notes that medial patellar luxation (where the kneecap pops inward) is more common in small and miniature breed dogs. Clinical signs generally start showing before the age of 1 year. The characteristic presentation is intermittent non-weight-bearing lameness of the affected hindlimb that resolves within a few steps -- often described as a "skipping" gait.

The American College of Veterinary Surgeons reports that patellar luxation is diagnosed in approximately 7% of puppies. The condition affects both knees in about half of all cases.

Breeds at highest risk in India: Spitz, Pomeranian, Toy Poodle, Chihuahua, Shih Tzu, Lhasa Apso, Maltese, Yorkshire Terrier, and Beagle are among the most commonly affected breeds. Larger breeds including Shar Pei and Flat-Coated Retrievers are also seeing an increasing incidence.

The condition is graded 1 through 4:

Grade 1: Kneecap can be manually moved out of position but returns on its own immediately.
Grade 2: Kneecap pops out occasionally during movement, causing the characteristic skip. Returns to position either on its own or with manipulation.
Grade 3: Kneecap is out of position most of the time but can be manually replaced.
Grade 4: Kneecap is permanently luxated and cannot be replaced manually.

Each time the kneecap slides out of its groove, it damages the cartilage lining the joint. Over time, this leads to osteoarthritis. Dogs with patellar luxation are also significantly more prone to cranial cruciate ligament tears.

Screening: Ask the breeder to confirm that the puppy has been examined for patellar luxation before sale. A simple hands-on orthopaedic examination at 8 weeks by a vet can detect Grade 2 and above. For toy breeds especially, this is a baseline expectation from responsible breeders.

Treatment: Grades 1 and early Grade 2 are often monitored. Grades 2 through 4 with clinical signs require surgical correction. The type of surgery trochleoplasty, tibial crest transposition, or a combination depends on the grade and the degree of bone deformity.

Dyschondroplasia: When Bone Growth Goes Wrong

Dyschondroplasia is a hereditary skeletal disorder in which the bones of the limbs, trunk, or head are underdeveloped or deformed.

According to the Merck Veterinary Manual, dyschondroplasia of the limbs is reported in Poodles and Scottish Terriers. The disorder in the trunk and head is seen in Alaskan Malamutes, Basset Hounds, Dachshunds, Poodles, and Scottish Terriers. In Malamutes, the condition is accompanied by anaemia.

Here is the interesting part: in some breeds, the body characteristics produced by dyschondroplasia are actively selected for by breeders. Among Basset Hounds, Dachshunds, and Pekingese, the short legs and long bodies that dyschondroplasia produces are considered desirable breed features. The same genetic mechanism that makes a Dachshund look like a Dachshund is, clinically, a bone growth disorder.

This is worth understanding before buying a Dachshund or Basset. Those breeds carry a higher risk of intervertebral disc disease and angular limb deformities precisely because of the bone growth pattern that defines their appearance. Their short, curved limbs place abnormal load on joints. Their long spines are more vulnerable to disc herniation. These are not accidents they are consequences of selectively breeding for dyschondroplastic traits.

Osteogenesis Imperfecta: Fragile Bones from Birth

Osteogenesis imperfecta (OI), sometimes called "brittle bone disease," is a rare inherited condition where a defect in collagen production makes the bones extremely fragile.

As the Merck Veterinary Manual describes, dogs with OI inherit very fragile bones and loose joints. The long bones tend to be slender with thin outer layers. A vet diagnosing the condition looks for calluses on the bones from repeated fractures. The whites of the eyes may also have a bluish tinge a secondary sign caused by the collagen defect affecting the sclera.

The professional Merck Manual notes that OI has been reported in Beagles, Collies, and Dachshunds, among other breeds. Genetic mutations in Type I collagen structure result in excessively fragile and osteopenic bones that are prone to pathological fractures and inefficient bone healing.

In practical terms: affected puppies fracture their bones from normal, gentle handling. The prognosis is poor. Puppies with severe OI are frequently euthanised due to the intensity of pain and the impossibility of normal activity. For affected dogs that survive, management focuses on preventing fractures and reducing pain. There is no cure.

For breeders: genetic testing for OI is now available and should be used before mating in any breed with known OI history.

Muscular Dystrophy in Dogs: Yes, It Exists

Most people associate muscular dystrophy with humans. It exists in dogs too, and it is inherited.

According to the Merck Veterinary Manual, several types of muscular dystrophy are seen in dogs. One type, similar to Duchenne muscular dystrophy in humans, has been seen in Golden Retrievers in the United States and Irish Terriers in Europe. Male dogs are more likely to be affected. Signs include muscular weakening, difficulty swallowing, a stiff gait, and loss of muscle mass. The disease is caused by the absence of a key protein required for normal functioning of muscle membranes. Some affected dogs also develop heart muscle disease.

A second type affects Labrador Retrievers in North America, Europe, and Australia. Dogs with this dystrophy develop a stiff gait, resist exercise, and begin to lose muscle mass as early as 6 months of age.

The Merck Manual's clinical veterinary edition notes that X-linked dystrophin-deficient muscular dystrophies have been described in numerous breeds, with specific genetic mutations identified in Golden Retrievers, German Shorthaired Pointers, Cavalier King Charles Spaniels, Japanese Spitz dogs, Rottweilers, and Brittanys.

For Indian dog owners: Golden Retrievers are one of the most popular breeds in Indian cities. Anyone purchasing a Golden Retriever puppy should ask whether the breeding male has been checked or genetic testing done in the breeding line. While this condition is not common, it is entirely genetic and preventable through responsible screening.

Wobbler Syndrome: Neck Vertebra Malformation in Large Breeds

Wobbler syndrome, or caudal cervical spondylomyelopathy, is a condition where abnormal development of the cervical (neck) vertebrae compresses the spinal cord. The dog develops a characteristic "wobbly" gait -- typically first visible as an unsteady, over-reaching stride in the hind legs.

According to the Merck Veterinary Manual, wobbler syndrome may be inherited and its most commonly affected breeds include Borzois, Basset Hounds, Doberman Pinschers, and Great Danes. Signs range from mild difficulty walking to paralysis of all four legs. Dogs often keep their neck flexed awkwardly downward.

The condition has two forms. The disc-associated form affects middle-aged Dobermans (typical onset around 7 years). The bony-associated form affects young giant breeds including Great Danes, Mastiffs, and Rottweilers, often appearing before 4 years of age.

Surgery can relieve pressure on the spinal cord but outcomes vary. The outlook for recovery is uncertain. Dogs with severe spinal cord compression that has been present for a long time may not fully recover even with successful surgery.

For Indian owners: Doberman Pinschers are frequently seen in Indian cities and have a definite hereditary predisposition. Prospective Doberman owners should ask breeders whether cervical spine screening has been done on parents.

Rare Structural Anomalies: Missing Toes, Fused Feet, Extra Digits

The Merck Veterinary Manual lists several rare but real congenital structural anomalies in dogs:

Apodia: Dogs born without feet.

Hemimelia: Born without certain bones in the limbs.

Ectrodactyly (Lobster Claw Defect): Split or missing toes. This creates an abnormal, cleft appearance to the paw.

Polydactyly: Extra toes. This is far more common and is particularly seen in Great Pyrenees. In that breed, double dewclaws on the hind feet are actually a breed standard requirement, making it a deliberately preserved congenital trait.

Syndactyly: Toes fused together.

Most of these are rare. Ectrodactyly is the most clinically significant because it can cause substantial lameness and requires surgical management. Polydactyly in breeds where it is not a standard feature (the extra dewclaws often seen on Labradors or German Shepherds, for example) may need to be removed to prevent injury.

The Calcium Trap: How Indian Pet Parents Are Accidentally Making Things Worse

This section is critical for every Indian dog owner bringing home a large-breed puppy.

One of the most widespread and harmful myths in Indian dog ownership is that large-breed puppies need supplemental calcium to build strong bones. The reality is the opposite.

Published research shows that excess calcium intake during the growth phase worsens the severity of hip dysplasia in genetically predisposed puppies. As explained in our blog Giving Calcium to Your Puppy? You Might Be Causing the Problem, studies on Great Dane litters showed that puppies fed excess calcium developed more severe hip dysplasia than their littermates on controlled diets. The same excess calcium has been shown to contribute to OCD and hypertrophic osteodystrophy (HOD).

Why does this happen? A puppy's gut absorbs calcium in direct proportion to how much is in its food. Unlike adult dogs, puppies do not have a reliable mechanism to stop absorbing calcium when they have had enough. So excess calcium floods the developing skeleton, disrupting the conversion of cartilage to bone and accelerating growth beyond what the developing joints can handle.

If your puppy is eating a complete and balanced commercial food labelled for growth or large-breed puppies, it already contains the right amount of calcium. Adding a calcium syrup or tablet on top creates excess. This is not a hypothetical risk vets across India see HOD, OCD, and angular limb deformities in puppies whose owners were trying to do the right thing.

What to do instead:

Feed a complete and balanced commercial diet formulated for large-breed growth.
Do not add calcium supplements unless your vet has identified a specific deficiency and directed supplementation.
If feeding a home-cooked diet (rice, chicken, dal), work with a vet nutritionist to ensure correct mineral balance -- chicken meat alone has a calcium-to-phosphorus ratio of roughly 1:16, far outside the 1.1:1 to 1.3:1 that growing bones need.

Breed-Specific Risk Table

Breed	High-Risk Conditions
German Shepherd Dog	Hip dysplasia, Wobbler syndrome, elbow dysplasia
Labrador Retriever	Hip dysplasia, elbow dysplasia, OCD, muscular dystrophy
Golden Retriever	Hip dysplasia, elbow dysplasia, OCD, muscular dystrophy, OI
Rottweiler	Hip dysplasia, elbow dysplasia, OCD, Wobbler syndrome
Great Dane	Hip dysplasia, OCD, Wobbler syndrome (bony form), OI
Doberman Pinscher	Wobbler syndrome (disc form), hip dysplasia
Dachshund	Dyschondroplasia (chondrodystrophy), OI, intervertebral disc disease
Basset Hound	Dyschondroplasia, angular limb deformities, Wobbler syndrome
Pomeranian	Patellar luxation
Spitz (Indian/Japanese)	Patellar luxation, muscular dystrophy (Japanese Spitz)
Shih Tzu	Patellar luxation
Poodle	Dyschondroplasia, patellar luxation
Alaskan Malamute	Dyschondroplasia with anaemia
Great Pyrenees	Polydactyly (breed standard), hip dysplasia
Beagle	OI (documented), patellar luxation

What to Ask a Breeder Before You Buy

You are spending significant money on a puppy. You have every right to ask these questions directly.

For any large breed (Labrador, GSD, Golden, Rottweiler, Great Dane):

"Do you have OFA or BVA hip scores for both parents?" Ask to see the certificates. Good hip scores in both parents significantly reduce, but do not eliminate, the risk.
"Have the elbows of both parents been assessed?" Elbow dysplasia screening is equally important and often overlooked.
"Is there any history of OCD in previous litters?" OCD has both genetic and nutritional components -- a history of it in the line is a warning sign.

For small and toy breeds (Spitz, Pomeranian, Shih Tzu, Toy Poodle, Beagle):

"Has the litter been checked by a vet for patellar luxation?" Grade 2 and above is detectable at 8 weeks.
"Have any puppies in previous litters needed orthopaedic surgery?" Honest breeders will tell you. Ask anyway.

For Dachshunds:

"Is the puppy's weight within the breed standard?" Overweight Dachshunds compound the structural stress of their chondrodystrophic skeleton.
"Are there any dogs in the previous two generations with disc problems or hind leg weakness?"

For Dobermans:

"Do you know if any dogs in the line have been diagnosed with Wobbler syndrome?"

Red flags:

A breeder who dismisses health questions or claims "this breed has no health problems"
No documentation of any parental health screening
Puppies priced well below market with no explanation
A breeder who sells through an agent with no direct contact

Managing a Dog With a Congenital Disorder

If you already have a dog with one of these conditions, or you buy a puppy and a condition is diagnosed, here is what responsible management looks like.

Weight management is the single most impactful intervention. Every extra kilogram puts measurable additional load on an already compromised joint. Getting your dog to and keeping them at an ideal body weight reduces pain and slows progression of osteoarthritis more effectively than most supplements.

Controlled exercise. High-impact activity jumping, intense running, stairs accelerates joint damage. Replace it with low-impact alternatives: leash walks on flat ground, swimming, or hydrotherapy if available in your city. Several veterinary facilities in Pune, Mumbai, Bengaluru, and Delhi now offer underwater treadmill therapy.

Joint supplements. Glucosamine and chondroitin support cartilage health and are safe for long-term use. They work best as preventive and early-stage support rather than as a rescue for advanced disease. Products like MOBILITY PLUS TABLET (S) and MEGAFLEX POWDER (S) both with confirmed discounts on Animeal -- can be incorporated into daily feeding routines. For dogs that resist tablets, powders sprinkled over food are often better accepted. A CANITONE JOINT SUPPORT TABLET is another consistently rated option for joint cartilage support at an accessible price.

Appropriate veterinary care. For conditions requiring surgery (severe hip dysplasia, OCD, Grade 3+ patellar luxation, Wobbler syndrome), timely referral to a veterinary orthopaedic surgeon matters. The longer a mechanical joint problem is left unaddressed, the more severe the secondary arthritis becomes.

Genetic counselling for breeding. If you are a breeder, a dog with a confirmed heritable condition should not be bred from. This is both ethically sound and, in some countries, increasingly a legal requirement. India does not yet have mandatory breeding health standards, but the veterinary and kennel club communities are moving in that direction.

FAQ

Can I prevent hip dysplasia in my Labrador puppy?
You cannot eliminate a genetic predisposition, but you can significantly influence severity. Keep your puppy lean during growth, avoid high-impact exercise and stairs before 12 months, feed a large-breed-appropriate diet without extra calcium, and have hip X-rays done at 12 to 18 months for a baseline assessment. A genetically predisposed dog managed well will have meaningfully better joints at age 5 than one that was allowed to be overweight and over-exercised.

My Spitz puppy occasionally holds up one back leg for a few steps. Is that normal?
That intermittent "skipping" gait is the classic presentation of patellar luxation. It is common in Spitz and Pomeranian breeds. Take your puppy to a vet for an orthopaedic examination. If it is confirmed as Grade 1 or 2, your vet will advise monitoring or, in Grade 2 cases with frequent episodes, surgical correction. Do not ignore it: each luxation episode causes cartilage damage and increases the long-term risk of osteoarthritis and cruciate ligament injury.

I was told by the breeder that both parents have "good hips". Does that guarantee the puppy will be fine?
No. Hip dysplasia is polygenic it involves many genes. Even two parents with certified good hips can produce a puppy with hip dysplasia, though the risk is much lower than from unscreened parents. Health screening of parents is the best available tool, not a guarantee.

My Dachshund is short-legged as a breed characteristic. Does that mean he has a disorder?
Technically yes dyschondroplasia, the bone growth abnormality that gives Dachshunds their short limbs and long backs, is a hereditary skeletal disorder. But it has been selectively bred to define the breed type. What this means in practical terms is that Dachshunds have a structurally higher risk of intervertebral disc disease than most other breeds, and keeping them lean, avoiding jumping, and using ramps instead of stairs are genuine management tools rather than optional extras.

At what age can osteochondrosis be diagnosed?
OCD typically shows up between 4 and 8 months of age, when the puppy is growing fastest. A puppy that is lame in a forelimb at this age should be assessed for OCD. X-rays may show early changes; CT scanning is more sensitive and increasingly available in Indian metros.